Emulsifiers and IBD: what the science says, and how to navigate
Carrageenan. Cellulose gum. Polysorbate 80. Mono- and diglycerides.
If turning food packets over has become a new family hobby since a Crohn's or colitis diagnosis, these names have probably crossed your path, usually with a warning attached. When it comes to emulsifiers and IBD, some of that concern is well founded.
The most useful thing to know from the start: "emulsifier" describes a job, not a substance. And ingredients doing the same job in a tub of ice cream don't necessarily behave the same way once they reach the gut. So whilst in an ideal world "emulsifier free" may be an optimum strategy, the reality is a lot more nuanced.
What are emulsifiers in food?
Oil and water don't naturally mix. Emulsifiers help them stay together, giving foods a smooth texture, a stable consistency and a longer shelf life. Many of the same ingredients also work as thickeners, stabilisers or gelling agents, which is why the terms blur together on labels and online.
Chemically, it's a surprisingly mixed family: seaweed extracts (carrageenan), modified plant cellulose (carboxymethylcellulose), seed and bacterial gums (guar, xanthan), phospholipids (lecithin), fat-based compounds (mono- and diglycerides) and synthetic surfactants (polysorbates).
UK/EU and US labels: UK and European labels often use E numbers - carrageenan is E407, cellulose gum E466, polysorbate 80 E433. US labels use the ingredient name instead, so look for "carrageenan", "cellulose gum" or "polysorbate 80".
How common are emulsifiers in everyday food?
Very. When researchers at King's College London reviewed nearly 13,000 products from the UK's four biggest supermarkets, just over half contained at least one emulsifier, and around half of those contained more than one. Lecithin and mono- and diglycerides were the most common (Sandall et al., 2023).
They also turn up in foods families choose with the very best intentions: gluten-free bread, dairy-free yoghurts, plant milks, nutritional drinks. A child avoiding gluten or dairy can end up eating more gums and stabilisers, simply because those are used to hold the alternatives together.
Why might emulsifiers matter in IBD?
It comes down to one of the gut's key structures: the mucus layer.
In the colon, a dense inner layer of mucus normally keeps the vast bacterial community at a respectful distance from the cells lining the gut wall. That separation is foundational. It allows the immune system to live alongside trillions of microbes without being constantly provoked.
In ulcerative colitis, bacteria have been found penetrating that normally impenetrable inner layer (Johansson et al., 2014). So anything that impacts that protective boundary further is worthy of attention.
In landmark mouse studies, two emulsifiers in particular - carboxymethylcellulose (CMC) and polysorbate 80 (P80) - shifted the microbiome, thinned the mucus, let bacteria move closer to the gut lining and triggered low-grade inflammation, or colitis in genetically susceptible mice (Chassaing et al., 2015). Tellingly, mice without gut bacteria were protected. The microbes weren't innocent bystanders; they were the go-betweens.
Other emulsifiers seem to work through quite different routes:
Polysorbate 80 changes the behaviour of Crohn's-associated E. coli in lab studies, helping them cross the specialised immune tissue of the small intestine (Roberts et al., 2010).
Carrageenan can switch on inflammatory signalling directly in human gut-lining cells, through an innate immune receptor called TLR4 (Bhattacharyya et al., 2008).
Xanthan gum is actually food for some gut bacteria. Many people carry microbes that break it down, creating a little microbial food chain (Ostrowski et al., 2022). Its effect may therefore depend on the gut microbes already present.
When researchers exposed human gut bacteria to 20 different emulsifiers in the lab, some caused marked disruption and others barely registered (Naimi et al., 2021). It just re-enforces - whilst they may broadly do the same job in food, they may have very different behaviours in the gut.
What do human studies show about emulsifiers in Crohn's and colitis?
In healthy adults: a tightly controlled feeding study gave a small group CMC for 11 days. It reduced microbial diversity and lowered beneficial short-chain fatty acids, and in a couple of participants bacteria moved into the mucus layer (Chassaing et al., 2022).
A Belgian trial of around 60 healthy adults found that several emulsifiers lowered short-chain fatty acids over four weeks, but none raised calprotectin or CRP. The carrageenan group did show a rise in one measure of gut permeability compared with their own starting point (Wellens et al., 2025).
In Crohn's disease: the UK ADDapt trial is the biggest piece of the puzzle so far. 154 adults with mild to moderately active Crohn's all followed a low-emulsifier diet with dietitian support. Half were given daily snacks containing carrageenan, CMC and P80, without knowing which group they were in. After eight weeks, 49% of the low-emulsifier group had a meaningful improvement in symptoms, compared with 31% of those receiving the emulsifiers, and more had a substantial drop in calprotectin (Bancil et al., 2025). Nutrient intake held up well and food-related quality of life improved (Buckley et al., 2025). The results have been presented at major gastroenterology meetings; the full peer-reviewed paper is still to come at the time of writing.
Not every trial agrees. A smaller Australian trial of 24 adults with active Crohn's involving the ileum compared high- and low-emulsifier diets, both built on healthy-eating principles. Both groups improved, with no difference between them (Fitzpatrick et al., 2025). It's small and short, so it doesn't cancel out ADDapt, but it's a useful reminder that the quality of the whole diet is of substantial importance. The emulsifiers also differed: ADDapt added back three specific higher-concern ones, while the Australian diets used emulsifiers as found across the everyday food supply, so potentially less focused on the more challenging ones.
In ulcerative colitis: the evidence so far is lighter. One very small trial of people in remission found that three of those given carrageenan capsules relapsed, compared with none on placebo, among just 12 who completed it (Bhattacharyya et al., 2017). Its methods have since been publicly challenged (McKim et al., 2019). Hopefully more trials will be done in time.
In children: there are no emulsifier trials yet. What we do have is intriguing. Exclusive enteral nutrition (EEN) is recommended as a first-line treatment for paediatric Crohn's, and the Crohn's Disease Exclusion Diet (CDED), a whole-food approach designed to reduce dietary components thought to affect the microbiome and gut barrier, emulsifiers among them, has been shown to work well in children too (Levine et al., 2019). Yet EEN works even though some formulas contain stabilisers. Neither approach isolates emulsifiers, and both point to the same truth: the whole dietary picture matters more than any single ingredient.
Even in a standard care perspective, many now consider it may be prudent to reduce processed foods containing CMC, polysorbate 80 and carrageenan in both Crohn's and colitis (Levine et al., 2020).
Crohn's vs ulcerative colitis: does it matter where in the gut the IBD is?
This is the kind of detail I like to go down into. Looking at what's really going on, where the challenge points are, and what mechanistically may be happening in the body. It's one of the most interesting and least discussed angles. It's key to how I pratice and crucial when we start to think about individualised and tailored support.
For now, there are no studies showing that a child with ulcerative colitis is more or less sensitive to emulsifiers overall than a child with Crohn's in the small intestine. But the biology suggests that the route by which an emulsifier could cause trouble may differ depending on where the inflammation sits. This can then in turn suggest situations where we may seek to be more cautious.
The colon: a mucus story
The colon relies heavily on that thick, organised mucus barrier. In active ulcerative colitis, goblet cells (the mucus makers) often struggle, mucus becomes thinner and patchier, and bacteria get closer to the gut wall.
Now add an emulsifier like CMC, which has been shown to thin mucus and bring microbes closer. The two mechanisms overlap in a way that's hard to ignore. It doesn't prove CMC will worsen a particular child's colitis, but it makes reducing it a sensible, low-cost step, especially during active disease.
The terminal ileum: a different kind of barrier
The small intestine has a thinner mucus layer by design, so nutrients can get through. It relies more on chemical defences: Paneth cells release antimicrobial proteins that keep bacteria in check, and Paneth cell dysfunction is closely linked with ileal Crohn's, including through genes such as NOD2 and ATG16L1.
The ileum is also home to Peyer's patches - immune sampling stations that deliberately let small amounts of gut contents through for inspection. Early Crohn's ulcers often appear right over them (Roberts et al., 2010).
This is where the polysorbate 80 research becomes especially relevant. Adherent-invasive E. coli (AIEC) are found in the ileal lining of a subset of people with Crohn's. In the lab, P80 doubled the movement of Crohn's-associated E. coli across human Peyer's patch tissue, while soluble fibre from plantain cut it by almost half (Roberts et al., 2010). A nice reminder that what we eat can work in both directions. 🍌
So the possible pathways look quite different:
Colon: mucus thinning → bacteria closer to the gut wall
Ileum: a shifted microbial environment → certain bacteria behaving more aggressively → interaction with a specialised immune barrier
Real life is rarely that simple
Crohn's can affect the colon, mucus problems occur in Crohn's too, and microbiome changes happen in UC. A child with ileocolonic Crohn's may have elements of both. These are differences in emphasis rather than completely separate mechanisms.
It's worth noticing that the Australian trial which found no benefit recruited people with ileal Crohn's specifically. It's far too small to draw conclusions from, but it's exactly the kind of detail it's worth looking at, and observing as more research emerges.
Activity may matter as much as the label
A severely inflamed colon with major mucus disruption is a very different environment from UC in deep remission with a restored barrier. The research reflects this: in active UC the inner mucus layer was highly penetrable to bacteria, while most people in remission had a barrier much like those without UC (Johansson et al., 2014).
So a useful question isn't simply "Crohn's or colitis?" It's where the inflammation is, how active it is, which parts of the barrier are under pressure, what microbial environment sits alongside it, and what biochemically may be impacting. That's what individualised advice actually means in practice.
Does timing matter? Flares, low-fibre phases and antibiotics
Very possibly. The same child's gut can be more or less resilient at different points in their IBD journey. And in particular:
During a flare, mucus production, tight junctions and repair processes are all under pressure. An exposure that affects the microbiome or mucus barrier may have a greater impact now than when in stable remission. So it's a very sensible time to reduce the higher-concern emulsifiers.
During low-fibre phases, such as a low-residue diet during a flare or with strictures, gut bacteria have less fibre to feed on. In mice, fibre-starved bacteria switch to feeding on the mucus layer instead (Desai et al., 2016). That doesn't make anyone emulsifier-sensitive, but it may be a moment to be a little more selective, and it's one more reason to rebuild fibre gently once the time is right.
After antibiotics or a gut infection such as C. difficile, the microbiome and barrier are still rebuilding. It's a reasonable time not to add unnecessary pressure.
Does the microbiome you start with matter?
It seems so. In the CMC feeding study, only some participants responded strongly. When researchers transferred each person's original gut bacteria into mice, bacteria from the strong responders produced far more inflammation when the mice were given CMC (Daniel et al., 2024).
The same ingredient may land very differently in two different guts. There's no clear test for this in clinic yet, although we can make some useful observations that can guide. But it's a powerful reminder of why a one-size list rarely fits.
Which emulsifiers are worth reducing in IBD?
In an ideal world we would have clean, natural food that didn't have any emulsifiers added. In reality though, that can be challenging to navigate, and in particular for anyone following a reduced diversity diet - like gluten or dairy free.
So, I've put this priority list together, to give a view - based on the balance of evidence seen to date, and to help make this more navigable at what can be a really challenging time.
Priority | Examples | Why |
Avoid whenever possible | Carboxymethylcellulose / cellulose gum (E466), polysorbate 80 (E433), carrageenan (E407, E407a) | Strongest mechanistic evidence, the three used in the ADDapt trial, and already flagged by international IBD experts |
Reduce where you have suitable swaps | Other polysorbates (E432-E436), other modified celluloses (E461-E469), mono- and diglycerides (E471) | Less direct evidence, and closely related compounds can behave very differently; not worth making a good diet much more restrictive |
Small amounts or infrequent use | Xanthan gum (E415) | Interesting microbiome effects but little direct evidence of harm in IBD; hard to avoid in gluten-free foods |
Lower priority | Lecithin (E322), pectin (E440), guar gum (E412), gum arabic/acacia (E414) | Some show effects in lab models, but human evidence of harm is weak or lacking, and several are fermentable fibres; the trade-offs usually outweigh the case for avoiding them |
How can families reduce emulsifiers without it taking over?
Use an app (e.g. Yuka - free to download) to help review a product's additives, great for getting around the small print. Use as a guide, as its overall score isn't designed with IBD in mind.
Look at the whole day, not just one packet. An emulsifier appearing once is different from the same gums turning up at breakfast, in a mid-morning yoghurt, a lunchbox sauce, an after-school bar and pudding. Often, swapping two or three frequently eaten products cuts exposure dramatically while keeping meals familiar.
Swap where it's easy. Many plant milks, yoghurts, creams and ice creams have carrageenan-free or CMC-free versions sitting on the same shelf.
Keep what's working hard nutritionally. If a fortified plant milk provides calcium, iodine, vitamin D and protein that a child won't reliably get elsewhere, removing it over a lower-priority stabiliser may do more harm than good. The same goes for the one gluten-free bread a child actually enjoys.
Protect safe foods. For a child with a limited diet, a small appetite or growth concerns, a trusted food is worth a great deal. Food is nutrition, but it's also routine, confidence, school lunches and fitting in with friends.
Cook simply when you can. Meals made from whole ingredients are naturally lower in emulsifiers, no label-reading required. It doesn't need to be every meal.
Make changes with support. Dietary changes are best alongside support - nutritional therapist, dietician etc, especially during EEN or CDED, or when weight and growth are a concern.
Aim for progress, not perfection. Being informed about an ingredient is very different from being frightened of it.
You don't have to work it all out alone. Weighing up research, ingredient lists, nutrition, growth and what a child will actually eat can feel a lot to get your head around. If it's starting to feel complex, personalised support can make a real difference - helping you focus on the few changes that matter most for your child, and let go of the ones that don't.
The gut lining and its mucus renew themselves constantly, and the microbiome is always adapting. Provide that system with good foundations - nourishing food, fibre when it's tolerated, rest, and the right support - and ease the stressors you reasonably can. That's how a gut, and a child, can thrive. 🌱
The short version
"Emulsifier" is a job title, not a single ingredient, and different emulsifiers behave very differently in the gut.
The strongest case for reducing exposure in IBD is for carboxymethylcellulose (E466), polysorbate 80 (E433) and carrageenan (E407).
A large UK trial in adults with active Crohn's showed benefit from a low-emulsifier diet; a smaller (restricted) Australian trial didn't show additional benefit over achieving a healthy diet. There are no emulsifier trials in children yet.
Where inflammation is presenting, the type of IBD, how active it is, the individual microbiome and timing all plausibly change which mechanisms matter most.
Lecithin, pectin, and gum arabic are lower priority for removal for most people.
Nutrition, growth and a child's relationship with food come first.
As parents this can feel pressured and tough. Be kind on yourself and take one step at a time. Reach out for help if need be.
Quick-fire FAQ
Do emulsifiers cause IBD? There's no evidence they do on their own. IBD develops from a mix of genetics, immune regulation, the microbiome and environment. Emulsifiers are one environmental factor being studied, alongside wider ultra-processed food patterns.
Which emulsifiers are most worth avoiding with Crohn's or colitis? The three with the strongest case for reducing are carboxymethylcellulose/cellulose gum (E466), polysorbate 80 (E433) and carrageenan (E407). Most others are a lower priority.
Does my child need an emulsifier-free diet? Not necessarily. Reducing the higher-concern ones where it's easy is sensible for many families. A strict emulsifier-free diet is rarely needed - check individual circumstances - and may backfire if it narrows an already limited diet. Talk to your practitioner for help with this.
Is carrageenan the same as poligeenan? No. Poligeenan (degraded carrageenan) isn't permitted in food, and some older, more alarming studies used it (EFSA, 2018). Food-grade carrageenan has its own open questions, which is why it sits in the higher-priority group.
Is xanthan gum bad for IBD? There's no good evidence it harms people with IBD. It's worth not letting it stack up across the day, but not worth losing a well-tolerated gluten-free bread over.
What about lecithin? Lower priority. Lab findings are mixed, but in the Belgian trial soy lecithin was included as a likely neutral option and didn't raise inflammatory markers in healthy adults (Wellens et al., 2025). There's currently little human evidence to justify cutting it out.
My child is on EEN. Do the additives in the formula matter? EEN is a well-established, effective treatment in its own right and may avoid the need for steroids. Stay with the plan your IBD team has set and look to make positive changes once EEN has completed.
Can a stool test show whether my child is sensitive to emulsifiers? Not currently. Research is exploring which microbiome features predict sensitivity, and we can gauge useful info on overall gut health and where mechanistically there may be challenges, but no test can reliably answer that yet.
Are emulsifiers listed on US labels? Yes, by name rather than E number - for example "cellulose gum", "carrageenan", "polysorbate 80" or "mono- and diglycerides".
Beyond the basics
For the science-curious. These are emerging, plausible ideas rather than proven clinical tools.
What bacteria do, not just who's there. In the CMC feeding study, the changes in bacterial species were fairly modest, but the chemistry altered noticeably: short-chain fatty acids and free amino acids fell (Chassaing et al., 2022). This then produced a very different biochemical environment for the gut lining, amplifying the result.
Same danger signals, different routes. In lab models of the human gut microbiome, CMC and P80 both raised levels of flagellin and lipopolysaccharide, bacterial molecules the immune system reads as warning signs, even though they reshaped the microbial community in different ways (Naimi et al., 2021).
Mucus-eaters aren't villains. Some bacteria naturally feed on mucus. Akkermansia muciniphila is a good example, and it's generally linked with a healthier barrier. The important factor is balance: whether mucus production keeps pace with microbial consumption.
FUT2 and the mucus menu. The FUT2 gene determines whether certain sugars are displayed on mucosal surfaces. People with two non-working copies, so-called non-secretors, have a different mucosal environment, and non-secretor status has been linked with Crohn's. We haven't seen evidence that non-secretors are more sensitive to emulsifiers. But if some emulsifiers act at the mucus-microbe interface, genes shaping that interface may be future pieces of the puzzle.
E471 isn't one thing. "Mono- and diglycerides of fatty acids" covers a family of compounds made from different fatty acids. When researchers tested a mono- and diglyceride mix alongside two individual E471 compounds, the mix and glyceryl oleate had no significant effect on gut bacteria, but glyceryl stearate tested on its own had a marked detrimental one (Naimi et al., 2021). Same E number, very different behaviour, and unfortunately a label can't tell you which you're getting.
The EEN paradox. If single additives always determined outcomes, EEN shouldn't work as well as it does. It changes food antigens, fibre, fat composition, microbial substrates and nutritional adequacy all at once. It reinforces the impact and power of the whole nutritional environment.
This article is for information purposes only. It's not a substitute for individual or medical advice from your child's medical team.
References
Bancil, A. et al. (2025) 'DOP097 Emulsifier restriction is an effective therapy for active Crohn's disease: the ADDapt trial', Journal of Crohn's and Colitis, 19(Suppl 1), p. i262. doi:10.1093/ecco-jcc/jjae190.0136
Bhattacharyya, S. et al. (2008) 'Toll-like receptor 4 mediates induction of the Bcl10-NFκB-interleukin-8 inflammatory pathway by carrageenan in human intestinal epithelial cells', Journal of Biological Chemistry, 283(16), pp. 10550-10558. doi:10.1074/jbc.M708833200
Bhattacharyya, S. et al. (2017) 'A randomized trial of the effects of the no-carrageenan diet on ulcerative colitis disease activity', Nutrition and Healthy Aging, 4(2), pp. 181-192. doi:10.3233/NHA-170023
Buckley, A. et al. (2025) 'P0757 Emulsifier restriction does not impair nutrient intake and improves food-related quality of life in active Crohn's disease', Journal of Crohn's and Colitis, 19(Suppl 1), pp. i1460-i1462. doi:10.1093/ecco-jcc/jjae190.0931
Chassaing, B. et al. (2015) 'Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome', Nature, 519, pp. 92-96. doi:10.1038/nature14232
Chassaing, B. et al. (2022) 'Randomized controlled-feeding study of dietary emulsifier carboxymethylcellulose reveals detrimental impacts on the gut microbiota and metabolome', Gastroenterology, 162(3), pp. 743-756. doi:10.1053/j.gastro.2021.11.006
Daniel, N. et al. (2024) 'Human intestinal microbiome determines individualized inflammatory response to dietary emulsifier carboxymethylcellulose consumption', Cellular and Molecular Gastroenterology and Hepatology, 17(2), pp. 315-318. doi:10.1016/j.jcmgh.2023.11.001
Desai, M.S. et al. (2016) 'A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility', Cell, 167(5), pp. 1339-1353. doi:10.1016/j.cell.2016.10.043
EFSA Panel on Food Additives and Nutrient Sources (2018) 'Re-evaluation of carrageenan (E 407) and processed Eucheuma seaweed (E 407a) as food additives', EFSA Journal, 16(4), e05238. doi:10.2903/j.efsa.2018.5238
Fitzpatrick, J.A. et al. (2025) 'Clinical trial: the effects of emulsifiers in the food supply on disease activity in Crohn's disease', Alimentary Pharmacology & Therapeutics, 61(8), pp. 1276-1289. doi:10.1111/apt.70041
Johansson, M.E.V. et al. (2014) 'Bacteria penetrate the normally impenetrable inner colon mucus layer in both murine colitis models and patients with ulcerative colitis', Gut, 63(2), pp. 281-291. doi:10.1136/gutjnl-2012-303207
Levine, A. et al. (2019) 'Crohn's disease exclusion diet plus partial enteral nutrition induces sustained remission in a randomized controlled trial', Gastroenterology, 157(2), pp. 440-450. doi:10.1053/j.gastro.2019.04.021
Levine, A. et al. (2020) 'Dietary guidance from the International Organization for the Study of Inflammatory Bowel Diseases', Clinical Gastroenterology and Hepatology, 18(6), pp. 1381-1392. doi:10.1016/j.cgh.2020.01.046
McKim, J.M. et al. (2019) 'A critical review of "A randomized trial of the effects of the no-carrageenan diet on ulcerative colitis disease activity"', Nutrition and Healthy Aging, 5(2), pp. 149-158. doi:10.3233/NHA-180051
Naimi, S. et al. (2021) 'Direct impact of commonly used dietary emulsifiers on human gut microbiota', Microbiome, 9, 66. doi:10.1186/s40168-020-00996-6
Ostrowski, M.P. et al. (2022) 'Mechanistic insights into consumption of the food additive xanthan gum by the human gut microbiota', Nature Microbiology, 7, pp. 556-569. doi:10.1038/s41564-022-01093-0
Roberts, C.L. et al. (2010) 'Translocation of Crohn's disease Escherichia coli across M-cells: contrasting effects of soluble plant fibres and emulsifiers', Gut, 59(10), pp. 1331-1339. doi:10.1136/gut.2009.195370
Sandall, A. et al. (2023) 'Emulsifiers in ultra-processed foods in the UK food supply', Public Health Nutrition, 26(11), pp. 2256-2270. doi:10.1017/S1368980023002021
Wellens, J. et al. (2025) 'Effect of five dietary emulsifiers on inflammation, permeability, and the gut microbiome: a placebo-controlled randomized trial', Clinical Gastroenterology and Hepatology (published online 2025). doi:10.1016/j.cgh.2025.08.005
Comments