Most people think of food additives as background noise.

A little stabilizer here. A little artificial sweetener there. Something to keep salad dressing smooth, ice cream creamy, bread soft, protein bars shelf-stable, and “zero sugar” drinks sweet enough to fool your tongue.

The problem is that your tongue is not the only thing paying attention.

Your gut microbes are also reading the ingredient list.

And unlike your taste buds, they don’t care whether something has calories, whether it is “natural,” or whether the label says “keto,” “low carb,” “light,” or “healthy.” They care about chemistry. They care about what reaches them. They care about whether a compound changes the mucus layer, alters bacterial behavior, shifts metabolism, or lets the wrong microbes get too close to the gut lining.

That is where emulsifiers and artificial sweeteners become interesting. Some additives appear mostly neutral, some may even behave like fermentable fibers, and some repeatedly show signals that they can disturb the gut microbiome, weaken the gut barrier, and alter metabolic health in susceptible people.

The most concerning names in the research are polysorbate 80, often written as P80, and carboxymethylcellulose, often written as CMC. In the artificial sweetener world, the biggest microbiome signal has been seen with saccharin, with additional evidence around sucralose and aspartame.

The science is not finished. It rarely is. But it is far enough along that “these compounds are biologically inert” is no longer a serious position.

First, what are emulsifiers?

Emulsifiers help ingredients mix that normally want to separate.

Oil and water are the classic example. Without an emulsifier, many sauces, dressings, desserts, packaged breads, plant milks, protein shakes, coffee creamers, and frozen foods would split, clump, collapse, or develop a texture that makes people back away slowly.

Food companies use emulsifiers because they work.

Common examples include:

Polysorbate 80, or P80
Carboxymethylcellulose, or CMC
Lecithins
Mono- and diglycerides
Xanthan gum
Guar gum
Pectins
Carrageenan
Maltodextrin, which is not always classified as an emulsifier but often shows up in the same ultra-processed neighborhood

The trap is assuming these are all the same because they share a job in food manufacturing. They are not.

“Emulsifier” describes function, not biology. That means a synthetic detergent-like compound and a fermentable plant fiber can both end up in the same broad category. That is like calling both a chainsaw and a butter knife “cutting tools.” Technically correct. Nutritionally useless.

The gut barrier is not just a wall. It is a negotiated border.

To understand why some additives matter, you need to understand the gut barrier.

Your colon is packed with bacteria. Many are useful. Some are opportunists. Some are fine at a distance but dangerous if they move into the wrong neighborhood.

Your body handles this with layers of separation.

The gut lining is covered by mucus. That mucus is not just slime. It is a controlled habitat. Some bacteria live in or near it. Others should be kept away from the epithelial cells underneath. Immune cells monitor the area. Microbial metabolites, including short-chain fatty acids, help keep the system calm.

When this barrier works, the gut is not sterile, but it is organized.

When it breaks down, bacteria and bacterial products can get too close to the lining. The immune system sees that as a threat. Inflammation rises. Metabolism can change. In genetically susceptible people, this may worsen inflammatory bowel disease risk or severity. In metabolically vulnerable people, it may contribute to insulin resistance, weight gain, or low-grade inflammation.

That is the basic concern with certain emulsifiers: they may change the relationship between microbes, mucus, and immune tone.

Polysorbate 80 and CMC: the two additives that keep showing up at the crime scene

The landmark study in this area came from Benoit Chassaing, Andrew Gewirtz, and colleagues. In mice, relatively low concentrations of P80 and CMC changed the gut microbiota, promoted microbiota encroachment into the mucus layer, increased inflammatory potential, triggered low-grade inflammation, and contributed to features of metabolic syndrome.

The most important part was not simply “mice got inflamed.”

The important part was mechanism.

Germ-free mice, which lack gut microbes, were largely protected from the harmful effects. When microbiota from emulsifier-exposed animals were transferred into other mice, the inflammatory and metabolic changes could be transferred too.

That tells us the microbiome was not just a bystander. It was part of the machinery.

In plain English, the emulsifier did not simply irritate the gut like sandpaper. It changed the microbial community in a way that made the gut environment more inflammatory.

That is a much more interesting problem.

And a much harder one.

What bacteria change?

Research on P80 and CMC has found changes in both microbial composition and microbial behavior.

Some studies report increases in groups with pro-inflammatory potential, including members of Enterobacteriaceae and Escherichia/Shigella-like taxa. These are not always pathogens in the classic “food poisoning” sense. The issue is that some members of these groups are very good at blooming during inflammation and feeding the cycle.

Other studies report decreases in bacteria associated with barrier support or anti-inflammatory activity, including Faecalibacterium, Akkermansia, and Bacteroides dorei.

Faecalibacterium prausnitzii is often discussed in inflammatory bowel disease because it is one of the major butyrate-producing bacteria in the human gut. Butyrate is a short-chain fatty acid that helps feed colon cells and supports regulatory immune function.

Akkermansia muciniphila is a mucus-associated bacterium. That sounds suspicious until you understand its job. In many contexts, Akkermansia is linked with improved barrier function and metabolic health. It appears to help maintain a healthier mucus ecosystem, although its behavior can depend on context, diet, and host condition.

Bacteroides dorei is another species that has been linked with anti-inflammatory potential in some studies.

P80 exposure has been associated with reductions in Akkermansia and Bacteroides dorei. That matters because removing barrier-associated and anti-inflammatory microbes may leave more room for bacteria that thrive in inflammation.

The gut does not just lose “good guys.” It may lose the traffic cops.

CMC and microbiota encroachment

CMC may be especially important because human data now exist.

In a controlled-feeding study, healthy adults consumed CMC for a short period. The researchers found changes in gut microbiota composition, reduced microbial diversity, depletion of fecal metabolites, and in some participants, evidence of microbiota encroachment toward the gut epithelium.

That phrase, “microbiota encroachment,” deserves attention.

It means bacteria moved closer to the gut lining than they normally should. Think of the mucus layer like the buffer zone between a crowd and a stage. The problem is not that people exist. The problem is when the crowd breaks the barrier and rushes the performer.

Your immune system does not enjoy crowd work.

CMC also reduced levels of metabolites linked to microbial function, including short-chain fatty acids and free amino acids. That does not automatically mean disease, but it suggests the microbial ecosystem changed quickly in response to the additive.

This is one reason CMC is not just “fiber-like” because it is chemically a cellulose derivative. Chemical ancestry is not destiny. The microbiome responds to structure, dose, accessibility, and ecological context.

P80 and sulfide-producing bacteria

P80 has been linked in some studies to increased sulfide-producing bacteria.

Hydrogen sulfide is complicated. At low levels, it can act as a signaling molecule. At high levels or in the wrong location, it can damage epithelial metabolism, impair butyrate oxidation, and contribute to inflammation. Microbiology loves nuance. Wellness influencers usually do not.

Sulfide-producing bacteria include groups such as Desulfovibrio and other sulfate-reducing bacteria, although different studies vary in how precisely they identify the organisms involved.

The concern is not that all sulfur metabolism is bad. The concern is that P80 may push the gut toward a microbial state where sulfide production, mucus disruption, and inflammation reinforce one another.

In animal models, P80 has also been linked to increased susceptibility to intestinal inflammation and promotion of colon tumor development under certain experimental conditions. That does not mean eating one packaged dessert gives you colon cancer. It means chronic exposure, in a susceptible host, may push the gut environment in a direction we should not casually dismiss.

The dose, the host, the baseline microbiome, and the rest of the diet all matter.

The microbiome decides who gets hit hardest

One of the most important points is individual variability.

Not everyone responds to emulsifiers the same way.

Some microbiomes appear resilient. Others are vulnerable. In experimental systems, the baseline microbiota can determine whether exposure to CMC or P80 produces a strong inflammatory response.

That makes sense. These additives are not acting on a blank surface. They are entering an ecosystem.

If your gut already has low microbial diversity, reduced butyrate producers, poor mucus regulation, low Akkermansia, or a bloom of inflammation-associated Proteobacteria, an additive may push harder. If your gut ecosystem is diverse, fiber-fed, and metabolically stable, it may absorb the hit.

This is why two people can eat the same processed food and have different outcomes.

One person shrugs. Another gets bloated, inflamed, dysregulated, or metabolically worse.

Artificial sweeteners: no calories does not mean no biology

Artificial sweeteners, also called non-nutritive sweeteners, were long treated as metabolically inert because they provide little or no usable energy to the human host.

That was always a narrow way to think.

Your body is not the only metabolic system in your body. Your microbiome also has metabolism. A compound can pass through you with minimal calories and still change bacterial growth, gene expression, metabolite production, epithelial signaling, or glucose handling.

The best-known study came from Eran Elinav, Eran Segal, Jotham Suez, and colleagues. They found that artificial sweeteners could induce glucose intolerance in mice through changes in the gut microbiota. Saccharin produced one of the strongest effects.

The key experiment again involved transfer.

When microbiota from sweetener-exposed mice were transplanted into germ-free mice, the recipient mice developed glucose intolerance. That means the altered microbiome carried the metabolic effect.

That is the part that should make people sit up.

It was not just “sweetener in, glucose response out.” It was “sweetener changes microbes, microbes change host metabolism.”

That is a different level of evidence.

Saccharin: the strongest early signal

Saccharin has shown some of the clearest microbiome-mediated effects.

In mice, saccharin exposure changed microbial composition and function, including enrichment of pathways involved in glycan degradation. Glycans are complex carbohydrates found in food and host mucus. When microbial glycan metabolism shifts, the downstream products can change too.

Some studies found increases in short-chain fatty acids such as acetate and propionate. That sounds beneficial at first because SCFAs are often good.

Here comes the nuance.

SCFAs are not magic fairy dust. Location, amount, host context, and metabolic state matter. Acetate and propionate can participate in host energy metabolism and may serve as substrates or signals involved in glucose and lipid production. In one context, SCFAs support gut health. In another, altered production may reflect a microbial state that contributes to metabolic dysfunction.

This is why “more SCFAs” is not automatically good. Biology is not a smoothie label.

Saccharin has also been associated with increases in Bacteroides and Clostridiales in some experimental settings. Those are broad categories. Some members are useful. Some are not. The important point is that the community and its functions changed in ways linked to glucose intolerance.

Human studies: responders and non-responders

The human data are more mixed than the mouse data, which is exactly what we should expect.

Humans are messy. We eat different diets, sleep differently, carry different microbiomes, take different medications, have different genetics, and lie about snacks. The last one is practically a clinical variable.

In a 2022 randomized trial, healthy adults consumed saccharin, sucralose, aspartame, or stevia for two weeks at doses below the acceptable daily intake. The researchers found that non-nutritive sweeteners could induce person-specific changes in the microbiome and glycemic responses.

Saccharin and sucralose had notable effects on glucose tolerance in some participants.

The most important finding was personalization. Some people responded strongly. Others barely changed. When microbiomes from human responders were transferred into germ-free mice, the mice tended to mirror the glucose responses of the human donors.

Again, the microbiome was not decoration. It helped explain the response.

This is the future of nutrition science, whether people like it or not: averages are useful, but they hide responders.

Sucralose: not as clean as the marketing

Sucralose is widely used because it tastes sweet, is low in calories, and survives processing. It is found in drinks, protein powders, bars, low-sugar desserts, and tabletop sweeteners.

Some human studies have found little effect of short-term sucralose exposure on glucose control or microbiome composition. That should be said clearly.

But other studies raise concerns.

A ten-week study in healthy young adults reported that sucralose consumption altered the gut microbiome and was associated with changes in glucose and insulin responses. Some experimental models also suggest sucralose may increase Proteobacteria or promote Escherichia coli expansion under certain conditions.

Proteobacteria are often treated as a red flag in microbiome research because blooms of Proteobacteria can reflect instability, inflammation, oxygen leakage into the gut, or ecological disruption. That does not mean every increase is catastrophic. It means you should pay attention.

With sucralose, the best interpretation is not “safe” or “toxic.” The best interpretation is: effects appear context-dependent, and some people may be more metabolically or microbially sensitive than others.

Aspartame: absorbed early, but still not irrelevant

Aspartame is often argued to be less likely to affect the colon microbiome because it is broken down and absorbed in the upper gut.

That is a reasonable point.

But “less likely” is not the same as “impossible.” Aspartame can still affect host metabolism, upper gut signaling, appetite pathways, microbial exposure to breakdown products, and systemic metabolic conditions that feed back into the gut.

In diet-induced obese rats, chronic low-dose aspartame changed microbial composition and increased fasting glucose, despite reduced calorie intake and less weight gain. It also impaired insulin-stimulated glucose disposal.

That result is a good example of why calorie math alone is incomplete.

A compound can reduce calories and still push glucose handling in the wrong direction.

Again, this does not prove that every person drinking a diet soda develops insulin resistance. It means artificial sweeteners need to be studied as biologically active compounds, not treated as invisible because they lack sugar.

What bacteria are involved with artificial sweeteners?

Across studies, artificial sweeteners have been linked with shifts in several microbial groups, including:

Lactobacillus
Bifidobacterium
Akkermansia muciniphila
Bacteroides
Clostridiales
Enterobacteriaceae
Escherichia coli
Escherichia/Shigella-like taxa
Proteobacteria

The pattern varies by sweetener, dose, host, diet, and study design.

Some studies report reductions in beneficial genera such as Lactobacillus and Bifidobacterium. These bacteria are often associated with carbohydrate fermentation, lactate production, immune modulation, and colonization resistance. They are not universally beneficial in every context, but reductions can be a sign that the ecosystem is shifting away from a more stable configuration.

Akkermansia muciniphila may also decrease in some additive-exposure settings. Because Akkermansia interacts with the mucus layer, depletion may matter for barrier health.

Increases in Escherichia/Shigella-like taxa or Proteobacteria are often interpreted as signs of dysbiosis or inflammatory potential. These bacteria can take advantage of disturbed gut environments. They are the microbial equivalent of people who show up when the bar fight starts.

The taste receptor angle

Artificial sweeteners do not only interact with microbes.

They can also interact with sweet taste receptors in the gut, including receptors involving T1R3. These receptors help regulate glucose absorption, incretin signaling, and insulin-related pathways.

This is one reason “it has no calories” is too simplistic.

Your gut is not a passive tube. It senses sweetness. It sends signals. It adjusts transporters and hormones. Artificial sweeteners can activate some of those pathways without delivering glucose in the usual way.

That mismatch may matter more in some people than others.

The xenobiotic metabolism angle

Another important concept is xenobiotic metabolism.

A xenobiotic is a compound foreign to the body. Drugs are xenobiotics. Environmental chemicals are xenobiotics. Many food additives can be thought of this way too.

Gut microbes are extraordinary chemists. They can activate, deactivate, transform, detoxify, or weaponize compounds that pass through the intestine.

That means two people can consume the same sweetener or emulsifier and produce different microbial metabolites from it.

This may explain why baseline microbiome composition predicts response. The question is not only “what did you eat?” It is also “what did your microbes do with it?”

That is where food additive research gets both fascinating and inconvenient.

Are all emulsifiers bad?

No.

This is where the conversation needs discipline.

Some emulsifiers look concerning. Others look neutral. Some may be beneficial because they behave more like fermentable fibers.

Xanthan gum

Xanthan gum is a microbial polysaccharide used as a thickener and stabilizer. It appears to be handled by specific gut microbes in industrialized populations.

Research suggests some gut bacteria have adapted to degrade xanthan gum. One bacterium from the Ruminococcaceae family can break down xanthan gum into smaller carbohydrates, and Bacteroides intestinalis can then use some of those breakdown products.

That may increase short-chain fatty acid production.

Animal studies also suggest xanthan gum can help maintain the microbiota during antibiotic exposure and increase resistance against Clostridioides difficile colonization.

So xanthan gum is not in the same bucket as P80 or CMC. It may be neutral or even beneficial in some contexts.

Lecithins

Lecithins are phospholipids, often derived from soy or egg. They are common in chocolate, baked goods, supplements, and processed foods.

In human gut microbiota models, lecithins appear to have less disruptive impact than many other emulsifiers. Some studies even suggest beneficial shifts.

Phosphatidylcholine, a major component of lecithin, has shown protective effects in some colitis models. That said, phosphatidylcholine metabolism can also feed microbial production of trimethylamine, which the liver converts to TMAO, a compound studied in cardiovascular disease. So this is not a cartoon hero story either.

Still, lecithins do not currently look like the main villain in the emulsifier-microbiome story.

Pectins and guar gum

Pectins and guar gum are often used as stabilizers, but they are also dietary fibers.

These are generally more favorable from a microbiome perspective because they can be fermented by gut bacteria into short-chain fatty acids. They may support microbial diversity, stool quality, and barrier function.

That does not mean every person tolerates them well. Some people with IBS or small intestinal bacterial overgrowth may experience gas, bloating, or discomfort from fermentable fibers.

But biologically, they are closer to “food for microbes” than “detergent-like disruption.”

Mono- and diglycerides

Mono- and diglycerides of fatty acids are more complicated. Some studies suggest they shift the microbiome but may have neutral or even beneficial metabolic effects in certain models. Others suggest the broader additive context matters.

The practical takeaway is not that mono- and diglycerides are a health food. They are not kale wearing a lab coat.

But they are not currently as concerning as P80 or CMC based on microbiome-disruption data.

Akkermansia: the mucus-layer specialist

Akkermansia muciniphila deserves its own section because it keeps showing up in this field.

This bacterium lives in close relationship with the gut mucus layer. In many studies, higher Akkermansia abundance is associated with improved metabolic health, better barrier function, and lower inflammatory tone.

A key study found that Akkermansia muciniphila could counteract some harmful effects of dietary emulsifiers on the microbiota and host metabolism. Daily administration helped protect against emulsifier-induced microbiome disruption and metabolic deregulation in experimental models.

That does not mean everyone should run out and buy an Akkermansia supplement.

The field is promising, but context matters. Akkermansia interacts with mucus. In the right ecosystem, that can support renewal and barrier health. In the wrong context, especially if mucus production is poor or inflammation is active, the story may be more complicated.

The better lesson is this: the microbes that maintain the mucus layer may be central to whether food additives harm you.

Feed the barrier. Do not just chase a probiotic.

What about intergenerational effects?

Animal studies suggest maternal consumption of emulsifiers such as P80 can alter offspring microbiota and increase susceptibility to colitis later in life.

That does not prove the same effect occurs in humans at normal dietary exposures. But it raises a serious question.

The early-life microbiome is not just a temporary microbial starter kit. It helps train immune development, gut barrier function, and metabolic programming. If maternal diet changes microbial transmission or early immune tone, the consequences may last longer than the exposure itself.

This is one of the reasons ultra-processed diets during pregnancy and early childhood deserve more attention. Not panic. Attention.

Panic is cheap. Mechanism is better.

So what should people actually do?

The goal is not to memorize every E-number or live in fear of salad dressing.

The goal is pattern recognition.

If your diet is mostly whole foods, high in fiber, rich in plants, and low in ultra-processed products, occasional exposure to additives is probably not the main thing determining your gut health.

If your diet depends heavily on low-calorie processed foods, protein bars, sugar-free desserts, shelf-stable sauces, packaged breads, diet drinks, and “healthy” ultra-processed snacks, your microbiome may be getting a steady stream of compounds that were approved largely through old toxicology frameworks.

Those frameworks often asked whether an additive poisoned cells or caused obvious organ damage.

They did not always ask whether it changed microbial ecology, mucus structure, immune tone, bacterial gene expression, fecal metabolomes, glucose tolerance, or responder-specific risk.

That is the gap.

Practical label advice

You do not need to become a food-additive monk. Nobody likes that person at brunch.

But you can be strategic.

Watch for frequent exposure to:

Polysorbate 80
Carboxymethylcellulose
Cellulose gum
Sodium carboxymethylcellulose
Artificial sweetener blends
Saccharin
Sucralose
Aspartame
Acesulfame potassium
Maltodextrin, especially in “sugar-free” or powdered products

Lower concern or potentially more favorable additives include:

Pectin
Guar gum
Xanthan gum
Lecithin
Some fiber-based stabilizers

This is not a perfect ranking. It is a risk map.

The bigger issue is frequency. A little additive exposure here and there is different from building your diet around engineered foods designed to be soft, sweet, creamy, shelf-stable, and impossible to stop eating.

Ultra-processed food is not just food with “chemicals.” All food is chemicals. The issue is that ultra-processed food often combines low fiber, high palatability, refined starches, industrial fats, emulsifiers, sweeteners, flavor enhancers, and texture modifiers into a product your ancestors would have classified as witchcraft with a barcode.

The microbiome reality check

Here is the cleanest summary.

Some emulsifiers, especially P80 and CMC, can disturb the gut microbiome in animal models and human experimental systems. They may promote inflammatory microbial behavior, reduce beneficial taxa, thin or disrupt the mucus barrier, and allow microbes to move closer to the gut lining.

Artificial sweeteners are not metabolically invisible. Saccharin has strong evidence for microbiome-mediated glucose intolerance in experimental models, and human studies show that responses to saccharin, sucralose, aspartame, and stevia can be highly personalized.

Not all additives are equal. Xanthan gum, pectins, guar gum, lecithins, and some mono- and diglycerides appear less concerning, and some may support beneficial microbial activity depending on the person and context.

The biggest takeaway is not “never eat additives.”

The takeaway is that food additives should be judged by microbiome biology, not just old-school calorie math or acute toxicity testing.

Your gut is an ecosystem. Additives are ecological inputs.

Some are probably harmless. Some may be helpful. Some look like they push the system toward inflammation, barrier disruption, or metabolic dysfunction in susceptible people.

And the hard truth is this: if a food needs five texture engineers and three sweetener systems to convince your body it is eating something real, your microbiome may eventually file a complaint.

Bottom line

The safest move is boring, which is how you know it is probably right.

Eat more intact plants. Get enough fermentable fiber. Limit ultra-processed foods that rely heavily on emulsifiers and artificial sweeteners. Pay attention to your own response. If a “healthy” sugar-free product leaves you bloated, craving more, or metabolically off, believe your biology before you believe the front of the package.

The microbiome does not read marketing claims.

It reads chemistry.

References

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