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The ubiquitous consumption of ultra-processed foods (UPFs) has been of concern, with one recent analysis of national data showing that children's intake of these ready-to-eat, highly refined foods rose dramatically from 1998 to 2018 and now constitute the majority of kids' daily calories. Interest is growing in the possible role these foods may play in the increasing global rates of inflammatory bowel disease (IBD), which have coincided with increasing consumption of UPFs in Western and Westernizing countries over the past few decades.

Ashwin Ananthakrishnan, MD, of Massachusetts General Hospital and Harvard Medical School in Boston, and colleagues conducted a prospective cohort study to explore the possible connection between UPFs and the risk of Crohn' disease (CD) and ulcerative colitis (UC), which was published last month in .

The team studied participants in three long-standing nationwide cohorts: the Nurses' Health Study (1986-2014), the Nurses' Health Study II (1991-2017), and the Health Professionals Follow-up Study (1986-2012). Altogether these groups comprised 245,112 participants and 5,468,444 person-years of follow-up.

Ananthakrishnan discussed the study's findings in the following interview with the Reading Room.

What prompted your group to do this study at this time?

Ananthakrishnan: There have been several recent mechanistic studies tying in various components of food processing to intestinal inflammation and negative changes in the microbiome. But there have been few human cohort studies examining this robustly. Despite the strong biological plausibility seen in experimental studies, epidemiologic evidence in support of an association between UPF intake and the risk of IBD has been lacking.

What, exactly, are UPFs?

Ananthakrishnan: UPFs are highly processed commercial foods that undergo many different layers of manipulation prior to consumption. While bread and cheese are generally considered processed foods, they are not considered ultra-processed. The latter usually include foods such as candy, sweetened breakfast cereals, soft drinks, ice cream, and sweet snacks.

There are several mechanisms through which UPF consumption may influence the development of IBD. First, UPFs may replace unprocessed or minimally processed foods that are rich in fiber. Second, UPFs contain additives that may promote intestinal inflammation, such as salt, artificial sweeteners, and commercial emulsifiers and thickeners.

What were the main observations of the analysis?

Ananthakrishnan: The main finding was that greater consumption of UPFs was associated with higher risk of CD, which was not unexpected given prior experimental studies. The increased risk of CD in those in the highest quartile versus the lowest quartile was almost double, with a hazard ratio of 1.70. This increased risk was not seen for UC, however.

A higher percentage of energy intake from UPFs was also associated with higher body mass index, higher total energy intake, lower physical activity, and lower scores on the , a measure of diet quality that may help prevent chronic diseases.

Throughout follow-up, participants in the highest quartile of UPF intake consumed a median of 46.4% of their total energy from UPFs, compared with 21.0% of participants in the lowest quartile.

In addition, a few food subgroups showed particularly strong positive associations with CD risk, including ultra-processed breads and breakfast foods, frozen or shelf-stable ready-to-eat/heat meals, sweet snacks and desserts, sauces, cheeses, spreads, and gravies.

This may partly be explained by the fact that items in these subgroups -- for example, white bread, cake, margarine, and mayonnaise -- are rich in emulsifying and thickening agents.

Are there any theories about why UPFs did not seem to boost UC risk?

Ananthakrishnan: There are many environmental factors that differ between CD and UC. The latter may be less driven by the changes in the microbiome or immune response induced by UPFs.

Was there any indication of a duration-linked effect associated with high UPF consumption starting early versus later in life?

Ananthakrishnan: We were not able to examine this question. Whether the risk of incident CD differs by the duration of UPF exposure and if avoiding UPFs is beneficial to those with an established disease requires further research.

What's the most important takeaway message for physicians and others?

Ananthakrishnan: Recognizing the impact of UPFs on inflammation in CD, it may be prudent to suggest a reduction in UPF intake in those at high risk for or with established IBD, though this was not a question specifically examined in our study. By avoiding UPF consumption, individuals might substantially lower their risk of developing CD, in addition to gaining other health benefits. Interventional studies are needed to answer this important question.

You can read the abstract of the study here, and about the clinical implications of the study here.