Anyone who has microscopic colitis (MC), knows how miserable the nights can be. If we're lucky enough to be able to finally get to sleep, an urgency may jolt us awake at 2 a.m., and after we drag our exhausted body back to bed, the ordeal may be repeated again an hour later. And then the next day, we have to deal with brain fog, fatigue, and the sense that our brain simply will not cooperate.

Most of us chalk it up to being tired, but new research suggests the story is considerably more complicated than that, and considerably more important.​

MC patients often search for explanations for the cognitive symptoms that accompany flares. The difficulty concentrating, the word-finding struggles, and the sense of mental slowness that remains even after bowel symptoms ease, can all be mystifying. As we suspect, inflammation, dehydration, and medication side effects all seem to be reasonable candidates.​

This research adds another contributing factor. The disrupted sleep issue itself may be directly impairing brain function, independent of any other factor. A person waking repeatedly through the night isn't merely tired — their brain may be missing the maintenance window it needs in order to function well.

There's a familiar sequence in MC whereby symptoms worsen, sleep becomes fragmented, fatigue deepens, and mental sharpness declines. Then after a flare resolves, and sleep improves, the cognitive fog often begins to lift, as well. Most patients notice this. Most clinicians acknowledge it. Until now, the mechanism has been poorly understood.​

This study doesn't prove that sequence in MC patients — these were mouse experiments, not clinical trials in people with gastrointestinal disease. But the biological pathway it identifies is entirely consistent with what human MC patients observe. Fragmented sleep disrupts NREM restoration. Disrupted restoration impairs cognition. When sleep improves, cognition improvement follows.

The broader significance of this research for MC patients isn't that scientists have found something wrong with our brains. It's that they've identified just how much the brain depends on uninterrupted deep sleep to function well, and how real the consequences are when that sleep is repeatedly corupted.

Many patients, understandably, focus treatment conversations on stool frequency, urgency, and abdominal symptoms. Those are the most visible and disruptive aspects of the disease. But this research is a reminder that nighttime symptoms carry a second cost — the cognitive impairment accumulated from night after night of fragmented sleep.

Protecting sleep, through effective treatment of active disease, careful attention to diet and timing, and open conversations with our care team about nighttime symptom issues, may matter as much for our daytime mental function as it does for our rest.

The exhaustion and brain fog that so many MC patients experience during flares are not imaginary, not simply a matter of attitude, and not something to be ignored. They appear to reflect a real biological deficit — one that improves when the underlying cause, disrupted restorative sleep, is addressed.​

That appears to be the most useful contribution this research has to offer people living with active MC — a clearer explanation for something we have always known to be true.

1. Driessen, K., Squarcio, F., Tononi, G. and Cirelli, C.. Induction of cortical on/off periods in awake mice fulfills sleep functions. Nature Neuroscience, (2026). Retrieved from https://www.nature.com/articles/s41593-026-02318-9

2. National Institutes of Health. (2026, June 8). Researchers trigger sleep’s restorative effect in parts of the awake brain. NIH, Retrieved from https://www.nih.gov/news-events/news-releases/researchers-trigger-sleeps-restorative-effect-parts-awake-brain?utm_source=join1440&utm_medium=email&utm_placement=newsletter&user_id=68a3102abf6d702e4e0e3f1f

The recognition that colonoscopy carries significant infection risk emerged primarily after multiple outbreaks involving contaminated endoscopes, particularly duodenoscopes used in specialized procedures. Investigators discovered that even when hospitals followed official cleaning protocols, bacteria could survive, hidden in microscopic crevices and biofilms within the instruments.​

A major Johns Hopkins analysis found infection rates of approximately 1.1 per 1,000 screening colonoscopies and 1.6 per 1,000 non-screening colonoscopies, with even higher rates for upper endoscopy. Some outpatient centers showed infection rates exceeding 100 times previous estimates. Other reviews estimated overall endoscopic infection rates between 0.2% and 0.37%, depending on procedure type and patient population.

These numbers represent a dramatic departure from the "one in a million" assurances patients received for years.

Significant improvements have occurred over the past decade. Hospitals now perform more rigorous post-cleaning culturing and monitoring than previously. Manufacturers have introduced redesigned scopes with removable end caps, partially disposable components, and improved channel access, particularly for high-risk duodenoscopes. Single-use disposable endoscopes are increasingly available, eliminating cross-contamination risk entirely. Enhanced sterilization procedures, and additional high-level disinfection steps have reduced some contamination rates.​

Despite these advances, serious problems persist. Contamination still occurs regularly. Biofilms remain difficult to eradicate completely. Most scopes are reused hundreds or thousands of times, and reprocessing quality varies widely between facilities. Importantly, some outbreaks occurred even when staff correctly followed manufacturer cleaning instructions, leading many experts to conclude that reusable scope design itself is fundamentally problematic.

The improvements are real and meaningful, but the problem is far from solved. Patients undergoing colonoscopy face substantially lower infection risk than a decade ago, but that risk remains measurably higher than medicine once claimed.

Beyond infection risks and bowel preparation concerns, MC patients face another potential problem that medical professionals rarely discuss — propofol, the sedative used during most colonoscopies, contains soybean oil and egg lecithin.​

The FDA and most anesthesia societies maintain that the refining process removes enough soy protein that soy-allergic patients face minimal risk. This conclusion, however, addresses primarily classic IgE-mediated anaphylactic soy allergy (the kind that causes immediate, life-threatening reactions). It does not adequately address the very different reactions many MC patients experience.

The medical literature largely asks: "Does propofol trigger life-threatening anaphylaxis?" But MC patients are asking a fundamentally different question: "Can it trigger immune activation, diarrhea, inflammation, or a flare?"​

These are not the same question, and the safety studies that reassure allergists about anaphylaxis risk were never designed to detect the delayed inflammatory responses characteristic of MC

Most anesthesia safety studies look for immediate allergic reactions: hives, airway compromise, or hypotension occurring during or immediately after the procedure. MC patients, however, often experience diarrhea hours later, inflammatory flares days later, histamine symptoms, or mucosal immune activation—outcomes that are rarely tracked or attributed to anesthesia exposure.​

This creates a massive blind spot. Gastroenterologists typically do not systematically follow patients after colonoscopy for delayed flares, and usually attribute post-procedure diarrhea to bowel prep, stress, or transient irritation. Delayed immune reactions may be substantially underreported simply because no one is looking for them.

During a colonoscopy procedure, patients are simultaneously exposed to bowel prep chemicals, dehydration, electrolyte shifts, mucosal irritation, microbiome disruption, sedation/anesthesia, and procedural mechanical trauma. Isolating propofol's specific contribution becomes extremely difficult.​

To answer this question properly, researchers would need studies tracking MC patients receiving propofol, monitoring symptom flares after colonoscopy, measuring delayed diarrhea and inflammatory markers, and assessing mast cell activation in food-sensitive populations. To our knowledge, those studies largely do not exist.

The FDA's position adequately addresses immediate allergic risk from highly refined soy oil in the general population. But MC patients may be experiencing delayed immune activation, mast cell responses, or inflammatory flares that current anesthesia safety frameworks were never designed to evaluate.​

The existing "safe for soy allergy" framework may not adequately address highly sensitive inflammatory bowel populations like MC patients. For patients with MC who know they react to soy, the standard medical reassurance that propofol is safe deserves skepticism based on real-world patient experience, even if formal studies haven't yet documented the problem.

Despite the lack of formal proof, the concern has biological merit. Colonoscopy preparations work by creating massive osmotic shifts, rapidly flushing intestinal contents, altering the mucosal environment, disrupting gut bacteria, stressing epithelial barriers, and causing intense water secretion into the bowel. For susceptible individuals, this aggressive process could theoretically damage the mucosal barrier, activate immune responses, alter gut permeability, and potentially trigger chronic inflammation.

Why? Because every one of the mechanisms resulting from exposure to colonoscopy preparations named above, is also present during MC reactions — quite a coincidence, to say the least. Obviously, an aggressive bowel cleanse checks multiple boxes as a potential trigger.​

But to illustrate once again how we all seem to respond differently to different stimuli, epidemiological evidence shows that more than a few MC patients achieve temporary remission following a cleanout/colonoscopy procedure, although in most cases, the remission fades away after a week or two.

Research into this question faces a fundamental obstacle — most patients undergo colonoscopy because they already have diarrhea or gastrointestinal symptoms. Researchers cannot easily determine whether bowel prep triggered MC or whether the patient had early undiagnosed MC before the procedure. This creates an intractable confounding problem that makes causal studies extremely difficult.​

The one scenario researchers could potentially study (the onset of chronic diarrhea following screening colonoscopy in previously asymptomatic individuals) represents a minority of cases and would require enormous sample sizes to detect statistically, because of MC's relatively low prevalence.
And to further complicate the problem, some individuals may have asymptomatic MC, prior to the colonoscopy.

A more plausible and likely more common scenario is that bowel prep triggers flares rather than causing new-onset MC. Patients with existing MC, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), mast cell disorders, or impaired mucosal barriers may be particularly vulnerable to symptom flares, microbiome disruption, increased intestinal permeability, and dehydration or electrolyte stress following aggressive bowel cleansing.​

This possibility is increasingly recognized clinically even though hard data remain limited. Many gastroenterologists have observed patients whose MC was previously well-controlled experiencing prolonged flares following colonoscopy preparation, suggesting the prep's disruptive effects can overwhelm compensatory mechanisms in compromised intestinal tissue.

For patients with established MC, who are scheduled for a colonoscopy, several practical issues should be considered. A paatient's MC diagnosis should be explicitly discussed with their gastroenterologist before the procedure, so that preparation can be individualized. Split-dose preparations may be better tolerated than single-evening preparations. Aggressive electrolyte and fluid replacement before, during, and after preparation may minimize disruption.

MC patients should consider whether the colonoscopy is truly necessary or whether symptom-based management would be appropriate, particularly if a recent colonoscopy confirming MC diagnosis has been performed. Missed diagnoses are common, but MC is virtually never mistakenly diagnosed if it doesn't exist. So if a “new” gastroenterologist insists on a repeat colonoscopy, that raises a red flag, because the procedure would be very unlikely to turn up any additional useful information. Yet many gastroenterologists facing a new patient try to talk the patient into a repeat colonoscopy, because it's typically a very profitable procedure. A repeat colonoscopy should be performed only if biopsy samples were not taken during a previous colonoscopy, or screening for polyps or cancer is needed.​

For patients without known MC undergoing a screening colonoscopy, who develop persistent diarrhea afterward, awareness that colonoscopy preparation might have triggered or unmasked intestinal inflammation is important. This doesn't mean avoiding necessary colonoscopies, but it does mean that new-onset persistent diarrhea following the procedure warrants evaluation rather than assumption that symptoms will resolve spontaneously.

Infection risks from a colonoscopy procedure are real and substantially higher than medicine once claimed. Current estimates suggest approximately 1 to 4 infections per 1,000 colonoscopies in many real-world settings, with higher risks in certain facilities and patient populations. Progress through improved cleaning methods, surveillance, scope redesign, and disposable technologies has meaningfully improved safety, but contamination problems have not been eliminated. The fundamental challenge of adequately sterilizing complex reusable instruments remains.

Regarding propofol sedation, the medical community has established that life-threatening anaphylactic reactions to refined soy oil are rare. However, this safety framework does not adequately address the delayed immune activation, mast cell responses, and inflammatory flares that MC patients commonly experience. Many MC patients who react to soy in their diet, report symptom flares following a colonoscopy, yet these delayed reactions fall outside the scope of anesthesia safety monitoring. The disconnect between official reassurances and patient experience suggests that current safety assumptions may be too narrow for highly food-sensitive inflammatory bowel populations.

Regarding MC and bowel preparation, the medical community currently lacks reliable data. There is no proven causal percentage, no definitive study establishing that bowel prep solutions cause MC, and insufficient research to quantify risk. However, biologically plausible mechanisms exist, and clinical experience suggests aggressive bowel cleansing may trigger or unmask disease in susceptible individuals. Whether it causes new-onset MC, or primarily triggers flares in existing subclinical disease, remains uncertain.

The questions of whether bowel prep contributes to MC and whether propofol triggers inflammatory responses in food-sensitive patients remain inadequately studied, representing significant gaps in gastroenterology research. Given that millions of colonoscopies are performed annually, and MC is now known to have substantial prevalence, rigorous investigation of these potential relationships would be valuable. Until such research exists, patients and physicians must make decisions based on incomplete information, balancing the genuine benefits of colonoscopy for cancer screening and diagnosis against uncertain but plausible risks in susceptible individuals.
​
Progress has been made on infection control, but the contamination problem, the propofol sensitivity issue, and the bowel-prep question all deserve continued attention, research investment, and honest acknowledgment of remaining uncertainties rather than premature reassurance that risks are negligible.

A major new study links popular sweeteners to faster cognitive decline. For microscopic colitis (MC) patients, there's a second layer of risk that most coverage isn't mentioning.

Many of us turned to artificial sweeteners and sugar alcohols years ago, to manage weight, control blood sugar, reduce calories, or simply because we were told they were a safer alternative to sugar. A major new study published in Neurology, the journal of the American Academy of Neurology, suggests that for at least some of those sweeteners, the "safer" assumption may have been wrong. And for MC patients, the concerns go beyond the brain.

Researchers at the University of Sao Paulo followed nearly 13,000 Brazilian adults with an average age of 52 for approximately eight years, tracking their consumption of seven widely used low- or no-calorie sweeteners and monitoring their cognitive function through repeated assessments of verbal fluency, working memory, word recall, and processing speed (American Academy of Neurology, 2025, September 3).1

The results were striking. People who consumed the largest total amounts of sweeteners experienced a 62% faster decline in overall thinking and memory abilities than those who consumed the least — a difference the researchers estimated was comparable to roughly 1.6 additional years of cognitive aging. Even those in the middle consumption group experienced a 35% faster decline, equivalent to about 1.3 extra years of aging.

The association was especially pronounced in adults under 60, and was stronger in people with diabetes than in those without it. Since people with diabetes are among the most frequent users of sugar substitutes (because they're advised to use them specifically to manage blood sugar) this finding is particularly significant.

The seven sweeteners studied were aspartame, saccharin, acesulfame K, erythritol, xylitol, sorbitol, and tagatose. Six of the seven — all except tagatose — were associated with faster cognitive decline. The researchers were careful to note that this was an observational study and could not prove that sweeteners caused the cognitive changes. Other factors could help explain the pattern. But the consistency and size of the association across nearly 13,000 people over eight years is not something to dismiss lightly.

The mechanisms aren't fully established, but several plausible pathways have been proposed in the research literature.

Aspartame is metabolized into methanol and then formaldehyde in the body, which can generate free radicals and oxidative stress. Some animal studies have found that aspartame at relatively low doses causes abnormalities in brain chemistry and learning deficits, and there is evidence that it may be able to breach the blood-brain barrier under some conditions (Ravn, 2025, October 10).2 Aspartame also produces phenylalanine as a breakdown product, which in large amounts can affect neurotransmitter balance.

A second and increasingly important pathway involves the gut-brain axis. Research has established that the gut microbiome communicates continuously with the brain through neural, immune, and endocrine signaling pathways. Disruption of the gut microbiome (called dysbiosis) can compromise the intestinal barrier, increase systemic inflammation through the release of bacterial endotoxins into the bloodstream, and trigger neuroinflammation that impairs cognitive function (Tana, Moffa, Tana, Ucciferri, and Moffa, 2025; Rundek et al. 2021).3, 4 Several artificial sweeteners, particularly sucralose and saccharin, have demonstrated bacteriostatic effects on gut bacteria, meaning they inhibit bacterial growth and can alter the composition of the microbiome in ways that tip it toward a pro-inflammatory state (Basson, Rodriguez-Palacios, and Cominelli, 2021; Xiaofa, 2014).5, 6​

as we'll discuss below.

What we know about the specific sweeteners:

Aspartame:
Found in diet sodas, many flavored drinks, tabletop sweeteners like Equal and NutraSweet, and thousands of processed food products. It was the sweetener most commonly discussed in the new Brazilian study's high-consumption group, and earlier research has linked it to oxidative stress and neurochemical changes in animals. The amount consumed by the highest intake group in the study was roughly equivalent to the aspartame in one can of diet soda per day.

Saccharin:
One of the oldest artificial sweeteners, found in Sweet'N Low and many processed foods. Epidemiological data from several countries has shown that spikes in IBD incidence have followed regulatory approval of saccharin in their markets — a correlation that has been noted in academic literature as potentially more than coincidental. Saccharin has demonstrated inhibitory effects on intestinal bacteria, and its decline in use in the late 1970s and early 1980s following cancer concerns was followed by a decrease in IBD rates in some regions.

Acesulfame K:
A high-intensity sweetener frequently used in combination with aspartame or sucralose to improve flavor in diet beverages and processed foods. It was among the six sweeteners associated with cognitive decline in the new study.

Sorbitol:
A sugar alcohol found naturally in some fruits and used widely in sugar-free candies, gum, baked goods, and medications. It was consumed in the largest quantity of any individual sweetener among the Brazilian study's participants, averaging 64 mg per day in the overall population. Sorbitol is also a well-established osmotic laxative — it draws water into the colon, which can cause bloating, cramping, and diarrhea even in people with healthy digestive systems (Mäkinen, 2016).7 For MC patients, this effect is relevant and serious.

Xylitol:
Another sugar alcohol, common in sugar-free gum, mints, and dental products. Like sorbitol, it's poorly absorbed in the small intestine, reaches the colon largely intact, and can cause osmotic diarrhea in sensitive individuals. Recent cardiovascular research has also raised concerns about xylitol's effects on platelet reactivity, suggesting potential links to increased clotting risk (Witkowski et al., 2023).8

Erythritol:
Generally considered the best-tolerated sugar alcohol from a gastrointestinal standpoint because most of it is absorbed in the small intestine before reaching the colon, minimizing the osmotic diarrhea effect that makes sorbitol and xylitol problematic. However, it was still among the six sweeteners linked to cognitive decline in the new study, and at high doses it can still cause nausea, bloating, and loose stools.

Tagatose:
The one sweetener in the study that was not associated with cognitive decline, and the exception is notable because tagatose has a meaningfully different biological profile from the others. It has a glycemic index of just 3 (compared to 65 for table sugar), acts as a prebiotic by generating short-chain fatty acids in the gut, and may actually support beneficial gut bacteria rather than disrupting them (Spinner, 2024, September 5; Durante et al., 2021).9, 10 Researchers at Tufts University recently developed a more efficient production method for tagatose, which may make it more widely available and affordable. It is already FDA-designated as generally recognized as safe (Love et al., 2025).11 For MC patients who need a sweetener, tagatose appears to be the most promising option currently available, although large quantities may still cause some GI discomfort in susceptible individuals, and human evidence on long-term effects remains limited.​

For most people, the cognitive findings in this study are the central concern. For MC patients, there's a second layer of risk that has received almost no attention in news coverage of the study. Several of these sweeteners have documented adverse effects on the gut that are especially dangerous for people with inflammatory bowel disease.

Sucralose, one of the most widely used sweeteners in the world, though not among the seven specifically studied in the new Brazilian research, has been shown in multiple animal studies to worsen gut inflammation in models of IBD, including both Crohn's disease and ulcerative colitis. It promotes dysbiosis, increases inflammatory markers, weakens the gut barrier, and stimulates the development of colonies of-invasive E. coli — the same pathogenic bacteria linked to soybean oil's effects on the gut (Rodriguez-Palacios et al., 2018).12 Research has also shown that sucralose worsens gut damage and promotes colitis-associated colorectal cancer risk in animal models (Li et al., 2020).13 About 10% to 15% of IBD patients report that artificial sweeteners worsen their symptoms — a figure that almost certainly understates the true proportion, since many patients don't connect their sweetener use to their symptoms.

Saccharin and acesulfame K have also been linked to IBD promotion through their inhibitory effects on intestinal bacteria. The concern is that these sweeteners remain in the gastrointestinal tract for extended periods, inhibit bacterial growth, reduce the bacterial populations that normally inactivate digestive proteases in the lower gut, and may thereby contribute to the protease-driven intestinal damage that's a feature of IBD pathogenesis.

Sorbitol and xylitol carry direct osmotic risks for MC patients. Both are classified as FODMAPs — fermentable carbohydrates that are poorly absorbed and highly fermentable in the colon. For someone whose gut is already compromised and whose colon responds to osmotic challenges with diarrhea and urgency, even moderate amounts of these sugar alcohols can trigger or worsen symptoms. Sorbitol in particular is a medically recognized laxative; it's not a dietary option that MC patients can safely use without caution.

The gut-brain connection adds another dimension. Research has increasingly established that gut dysbiosis can drive neuroinflammation through the gut-brain axis — that is, a disrupted and inflamed gut can contribute to cognitive impairment through systemic inflammation that reaches the brain. MC patients already have a disrupted gut environment and often experience brain fog that correlates with disease activity. Sweeteners that further disrupt the gut microbiome could theoretically worsen both gut symptoms and the cognitive effects they contribute to — a compounding problem rather than two separate ones.​

The Brazilian study's lead author specifically noted that more research is needed on alternatives such as applesauce, honey, maple syrup, and coconut sugar.1 None of those were studied, and for MC patients some of them carry their own risks depending on individual tolerance. Honey and maple syrup contain fructose and other sugars that can be problematic during flares. Applesauce is tolerated by many MC patients but contains sorbitol naturally — a consideration for those who are particularly sensitive.

Stevia and monk fruit were not included in the Brazilian study and were not among the sweeteners linked to cognitive decline. Neither has been associated with the gut dysbiosis effects documented for sucralose and saccharin, though animal research on stevia and the gut microbiome has produced mixed results that are not yet conclusive in humans. For MC patients who need a sweetener during remission, stevia appears to be one of the lower-risk options based on current evidence, as does tagatose — with the caveat that large amounts of either may not be well tolerated by everyone.

The picture that emerges from this research is that most of the commonly used sugar substitutes carry risks we weren't fully informed about when we started using them. Six of the seven sweeteners examined in a rigorous eight-year study of nearly 13,000 people were associated with measurable cognitive decline. Several of those same sweeteners have independent evidence linking them to gut dysbiosis, worsened IBD symptoms, and intestinal barrier damage. And the population most frequently advised to use sugar substitutes — people with diabetes — is the same population in which the cognitive effects appear to be strongest.

For MC patients, this isn't an abstract concern. Many of us use these sweeteners daily in beverages, medications, and processed foods, often without realizing they're there. They appear on labels under multiple names and are present in products that don't advertise themselves as sugar-free.

The most practical steps we can take are to read labels carefully and identify which sweeteners we're currently consuming, give particular priority to avoiding sorbitol, xylitol, saccharin, sucralose, and acesulfame K, consider shifting to tagatose or stevia as primary sweeteners if we need one, and discuss with our care team whether our current sweetener use is consistent with our gut health goals.
​
As with so many things in MC management, the safest approach is the most whole-foods-based one — meaning that reducing our dependence on sweetened products of any kind, artificial or otherwise, is probably the most protective step we can take for both our gut and our brain.

1. American Academy of Neurology. (2025, September 3). Study links high intake of artificial sweeteners to faster cognitive decline. Retrieved from https://www.news-medical.net/news/20250903/Study-links-high-intake-of-artificial-sweeteners-to-faster-cognitive-decline.aspx

2. Ravn, C. (2025, October 10). Does Aspartame Cause Demential? Memory Loss, Sweeteners & Daily Impact. Retrieved from https://optoceutics.com/does-aspartame-cause-dementia-alzheimers-memory-loss-artificial/?srsltid=AfmBOopUu25hEibVByI5O-F93d6bWxJT3mS80vs5FkdYTYF-sYYJRxdt

3. Tana, C., Moffa S, Tana, M., Ucciferri, C., and Moffa, L. (2025). Gut Microbiota, Mild Cognitive Impairment and Dementia: A Systematic Review. Neurology International, 17(10). 155. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC12566805/

4. Rundek, T., Roy, S., Hornig, M., Cheung, Y. K., Gardener, H., DeRosa, J., . . . Sacco, R. L. (2021). Gut permeability and cognitive decline: A pilot investigation in the Northern Manhattan Study. Brain Behavior & Immunity — Health, 12:100214. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC8186438/

5. Basson, A. R., Rodriguez-Palacios, A., and Cominelli, F. (2021). Artificial Sweeteners: History and New Concepts on Inflammation. Frontiers in Nutrition, 8:746247. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC8497813/

6. Xiaofa, Q. (2014). May artificial sweeteners not sugar be the culprit of dramatic increase of inflammatory bowel disease in China? Chinese Medical Journal, 127(17) Retrieved from https://mednexus.org/doi/pdf/10.3760/cma.j.issn.0366-6999.20140673

​7. Mäkinen, K. K. (2016). Gastrointestinal Disturbances Associated with the Consumption of Sugar Alcohols with Special Consideration of Xylitol: Scientific Review and Instructions for Dentists and Other Health-Care Professionals. International Journal of Dentistry, 2016:5967907. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC5093271/

8. Witkowski, M., Nemet, I., Alamri, H., Wilcox, J., Gupta, N., Nimer, N., . . . Hazen, S. L. (2023). The artificial sweetener erythritol and cardiovascular event risk. Nature Medicine, 29, pp 710–718. Retrieved from https://www.nature.com/articles/s41591-023-02223-9

9. Spinner, J. (2024, September 5). Tagatose sweetens with prebiotic benefits: ASR Group. Snack Food & Wholesale Bakery, Retrieved from https://www.snackandbakery.com/articles/112030-tagatose-sweetens-foods-with-lower-gi-and-prebiotic-benefits-asr-group

10. Durante, M., Sgambellone, S., Lucarini, L., Failli. P., Laurino, A., Collotta, D., . . . Collino, M. (2021). D-Tagatose Feeding Reduces the Risk of Sugar-Induced Exacerbation of Myocardial I/R Injury When Compared to Its Isomer Fructose. Frontiers in Molecular Biosciences, 8:650962. Retrieved from https://pmc.ncbi.nlm.nih.gov/articles/PMC8076855/

11. Love, A., Toomey, C., Kumar, A., Kashyap, S. N., Santhamoorthy, D. K., Muthuraj, L., . . . Santos, C. N. S. (2025). Reversal of the Leloir pathway to promote galactose and tagatose synthesis from glucose. Cell Reports Physical Science, 6(12). 102993. Retrieved from https://www.cell.com/cell-reports-physical-science/fulltext/S2666-3864(25)00592-2

12. Rodriguez-Palacios, A., Harding, A., Menghini, P., Himmelman, C., Retuerto, M., Nickerson, K. P., . . . Cominelli, F. (2018). The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn's Disease-Like Ileitis. Inflammatory Bowel Diseases, 24(5). pp 1005–1020. Retrieved from https://pubmed.ncbi.nlm.nih.gov/29554272/

13. Li, X., Liu, Y., Wang, Y., Li, X., Liu, X., Guo, M., . . . Jiang, M. (2020). Sucralose Promotes Colitis-Associated Colorectal Cancer Risk in a Murine Model Along With Changes in Microbiota. Frontiers in Oncology, 10:710. Retrieved from https://pubmed.ncbi.nlm.nih.gov/32582527/

When a label says avocado oil but the bottle contains soybean oil, microscopic colitis (MC) patients pay a price that goes well beyond the extra money spent at the checkout.

Many of us with MC have switched to avocado oil products in recent years, drawn by the promise of a clean, gut-friendly fat that avoids the seed oils we've learned to be cautious about. We pay more for chips, mayonnaise, and salad dressings labeled "made with avocado oil." We read the ingredient list, see avocado oil listed as the only oil, and feel confident we're making a safe choice.

A new study from the University of California, Davis suggests that confidence is very likely misplaced, and for MC patients sensitive to soy, the consequences can be more than financial.

Researchers at UC Davis purchased 54 packaged food products that listed avocado oil as the only oil ingredient — chips, mayonnaise, and salad dressings, and subjected them to chemical analysis. The results were stark. 89% of the products showed signs of adulteration with cheaper oils, most commonly soybean oil. One sample appeared to contain essentially no avocado oil at all (Godoy, 2026, July 21).1

The findings broke down by product category in a way that should concern anyone relying on these labels. Among chips labeled as made with avocado oil, 93% were adulterated. Among mayonnaises, 71% failed — and when U.S.-made products were examined separately, that figure climbed to 100%. Every single salad dressing product tested was adulterated (Quinton, 2026, July 15).2

Critically, price offered no protection. Products at the higher end of the price range were no more likely to be authentic than cheaper ones. Consumers paying a premium for what they believed was a cleaner oil were being misled just as thoroughly as anyone else.

For comparison, the same researchers tested 20 packaged food products made with olive oil. Only one showed signs of adulteration. As lead researcher Selina Wang, a professor of food science at UC Davis, put it: "So this is largely an avocado oil product problem."

This latest study is actually the third time in six years that UC Davis researchers have documented serious authenticity problems in the avocado oil market. A 2020 study found that 82% of commercially bottled avocado oils were either rancid or adulterated with other oils. A follow-up found similar problems with private-label products. What the new 2026 research confirms is that the fraud didn't clean itself up as the market grew — it expanded right alongside it, moving from bottled oils into the rapidly growing category of packaged foods that trade on the avocado oil label.

The economics make the incentive obvious. Pure avocado oil costs roughly $4 to $5 per pound. Soybean oil costs $0.50 to $1.50. The label premium that consumers pay for avocado oil products is real. The oil itself often isn't.

Investigators haven't been able to pinpoint exactly where in the supply chain the substitution typically occurs, whether at the level of the oil supplier, the ingredient processor, or the food manufacturer. What's clear is that the problem is systemic and that it doesn't leave a detectable trace on the label.

For the general public, buying adulterated avocado oil is primarily a consumer fraud issue — paying premium prices for an inferior product. For MC patients, it can be something considerably more serious.

Soy sensitivity is one of the most common food intolerances in the MC community. According to data shared by members of the Microscopic Colitis Foundation discussion forum, more than half of us are sensitive to soy proteins and related compounds. This figure is consistent with the broader pattern of MC-associated food sensitivities, which also include gluten and casein, and which appear to arise from the increased intestinal permeability (commonly called "leaky gut"), that accompanies the disease. Once the gut barrier is compromised, food proteins that would ordinarily be processed normally can cross into the intestinal wall and trigger an immune response.

Soybean oil presents a somewhat different issue than soy protein. Highly refined soybean oil theoretically contains very little soy protein and is sometimes considered safe for people with soy allergies. However, research on this point is not fully settled, and MC patients react to soy through immune pathways that may not follow the same rules as classic IgE-mediated soy allergy. Interestingly, there is now direct research evidence that soybean oil itself, independent of its protein content, may promote intestinal inflammation through a separate mechanism.

Soybean oil is composed of up to 60% linoleic acid, an omega-6 fatty acid. A research team at UC Riverside found that mice fed a diet high in soybean oil were significantly more susceptible to developing colitis. The mechanism involves linoleic acid's effect on the intestinal endocannabinoid system — it reduces levels of beneficial endocannabinoids in the gut, weakens the intestinal barrier, decreases beneficial bacteria, and promotes colonizing by-invasive E. coli, a strain of bacteria that has been linked to IBD in humans (Pittalwala, 2023, July 3; Deol, et al., 2023).3, 4

Americans already derive far more of their daily energy from linoleic acid than their bodies need — as much as 10%, against a requirement of just 1 to 2%. For MC patients who are already dealing with a compromised intestinal barrier, adding a hidden source of high-linoleic-acid oil through products that are supposed to be free of soybean-oil, compounds a risk that most of us aren't even aware we're taking.

Avocado oil, by contrast, is composed primarily of oleic acid, a monounsaturated omega-9 fat with a very different biological profile. It doesn't carry the same pro-inflammatory omega-6 overdose that makes soybean oil a concern for gut-sensitive individuals. When we choose avocado oil products, that difference is part of what we're paying for. The adulteration findings suggest we're usually not getting it.

The honest answer is that there's no easy solution. Short of having the oil in every product we buy independently tested, which isn't practical, we can't verify authenticity from a label alone, regardless of how confidently the packaging states "made with 100% avocado oil."

Bottled avocado oil from brands with documented third-party testing and supply chain transparency is more likely to be authentic than unverified packaged food products. If we're cooking at home with avocado oil, sourcing from a reputable bottled brand and preparing our own chips, dressings, and sauces gives us considerably more control than trusting a commercial product.

Among packaged foods, the adulteration problem appears worse in some categories than others. The UC Davis study found that salad dressings were uniformly adulterated and chips were nearly so. If we choose to buy these products at all, rotating brands and staying alert to any symptom changes after introducing a new product is a reasonable precaution.

For those of us who react to soy, the safest position, although frustrating, is to treat most commercially packaged "avocado oil" products with the same caution we'd apply to a product with soy listed on the label, at least until the industry develops and enforces meaningful authenticity standards.

The Avocado Oil Manufacturers Association, founded in 2025, has acknowledged the authenticity problem and expressed intent to address it, pointing to the olive oil industry as a model. It took years of published research, public pressure, and eventually, coordinated industry standards, before olive oil adulteration rates dropped to the relatively low levels seen today. The avocado oil industry appears to be at an early stage of that same process.

In the meantime, the burden falls on consumers, as it usually does, to navigate a marketplace where the label and the contents of the package don't reliably match. For MC patients who are already working hard to identify and eliminate foods that trigger symptoms, discovering that a product we trusted has been silently adulterated with one of our most problematic intolerances is a legitimate health concern, not just a shopping inconvenience.

1. Godoy, M. (2026, July 21). Is that food really made with 100% avocado oil? Likely not. MPR, Retrieved from https://www.npr.org/2026/07/21/nx-s1-5902084/avocado-oil-health-fraud-study

2. Quinton, A. (2026, July 15). That Avocado Oil Chip You’re Eating May Not Be Made With Pure Avocado Oil. University of California, Davis, Retrieved from https://www.ucdavis.edu/food/news/avocado-oil-chip-youre-eating-may-not-be-made-pure-avocado-oil

3. Pittalwala, I. (2023, July 3). Widely consumed vegetable oil leads to an unhealthy gut. University of California at Riverside, Retreived from https://news.ucr.edu/articles/2023/07/03/widely-consumed-vegetable-oil-leads-unhealthy-gut

4. Deol, P., Ruegger. P., Logan, G.D., Shawki, A., Li, J., Mitchell, J. D., . . . Sladek, F. M. (2023). Diet high in linoleic acid dysregulates the intestinal endocannabinoid system and increases susceptibility to colitis in Mice. Gut Microbes, 15(1). 2229945. Retrieved from https://pubmed.ncbi.nlm.nih.gov/37400966/

Because PAR2 continues signaling inside endosomes where traditional drugs cannot reach, researchers developed nanoparticles that deliver PAR2 blockers directly into endosomes.

How the nanoparticles work:
These engineered nanoparticles act as "Trojan horses":​

1. They are swallowed by intestinal cells and sensory neurons
2. Instead of escaping endosomes (like most drug carriers), they deliberately remain inside
3. They release a PAR2-blocking drug (AZ3451) precisely where the receptor is firing
4. Pain signals stop at their source​

Results in animal studies show

• long-lasting, powerful pain relief
• Normalization of pain-related behavior
• Reduction of inflammation
• Minimal systemic absorption (much safer than opioids or NSAIDs)

This represents a first-in-class pain therapy targeting intracellular receptors—a completely new approach to managing gut pain.

If this nanotechnology translates successfully to human trials, MC patients could have access to:

• Targeted pain relief without systemic side effects
• Anti-inflammatory effects at the cellular level
• No risk of addiction (unlike opioids)
• No GI damage (unlike NSAIDs, which can trigger MC flares)
• Long-lasting relief from a single dose

​
This could be transformative for the approximately 40% of MC patients who struggle to achieve stable remission with current medications.

​Researchers are now exploring engineered probiotics that secrete PAR2-deactivating enzymes. If successful, such probiotics could:

• Reduce pain naturally
• Restore intestinal barrier function
• Decrease inflammation
• Provide long-term disease control
• Offer a non-drug therapy for MC​

This aligns perfectly with existing MC treatment approaches that emphasize specific probiotic strains like Bifidobacterium infantis 35624, Lactobacillus plantarum 299v, and Saccharomyces boulardii.

These findings do not demonstrate that gut pain, once initiated, is "locked on" simply because PAR2 activation becomes "stuck on". It's more complicated than that, as you will see below.

​This was not part of the original studies cited above, of course, since the studies were designed to promote the development of an expensive medication (or drug) to be used for resolving gut pain. But as most of us are aware, the elimination of inflammatory foods from the diet can restore not only proper digestion, but microbiome balance. And most importantly, it can stop the pain associated with MC.

The fact that the PAR2 recepters get “stuck on” is irrelevant if the inflammation that is causing the activation of those receptors is suppressed, and this can be done by making the proper diet changes to eliminate the inflammation. After that, the pain cycle will naturally stop.

The sensory nerve endings that are responsible for sensing pain in the gut are called nociceptors, and they're a major target for the drugs discussed by the researchers. Endosomes in nociceptors typically last a few hours, up to maybe 24 hours. The descriptions in some of the articles discussing this research leave the impression that the endosomes last much longer, since the pain signaling they produce is "stuck on".

But that interpretation is misleading, because sustained endosomal signaling is necessary for prolonged pain signals, and the only way that the signaling can last for extended periods (days, or longer) is if the endosomes are continually replaced as they cycle out, and this requires that the bacteria must continue to produce the protease that activates the PAR2 receptors.

If the inflammation cycle that triggers the gut pain can be broken by an anti-inflammatory diet, for example, then the prolonged signaling by the PAR2 receptors will dissipate as the inflammation level declines in response to the diet changes.

​Although the PAR2 pain receptors may get "stuck on", as stated by Dr. Nigel Bunnett's team in their research findings — in the long run, this is irrelevant. If they were actually "stuck on" for the long-term, an elimination diet could not eliminate the pain symptoms of MC. To the contrary, a safe diet apparently results in the reduction of bacterial protease production, and lower PAR2 activation, because a safe diet can eliminate not only all the clinical symptoms of MC, but it will eventually restore normal histology to the cells of the colonic epithelia.

The key distinction is this:
A safe diet does not directly “switch off PAR2 receptors”, — it removes the foods and conditions that cause PAR2 activation — which indirectly leads to PAR2 downregulation and mucosal healing (despite the researchers insinuations that the receptors become "stuck on" for the long-term.

So diet is fully capable of normalizing these pathways for the following reasons:

1. The gut microbiome is primarily determined by diet. This is one of the strongest findings in all of gut science. The foods you eat determine which bacterial species survive. Removing inflammatory foods changes the ecological environment. Microbiome shifts occur within 48–72 hours after dietary change.

2. Bacterial protease production depends on which bacteria are present. Bacterial serine proteases (the molecules that activate PAR2) are produced by specific species, such as:

• Enterobacteriaceae
• Bacteroides fragilis
• Certain Proteobacteria
• Dysbiotic Clostridia

When our diet removes the substrate that supports these organisms (certain proteins, emulsifiers, carbohydrates, and additives, for example), their population drops dramatically, and there will be:

• Fewer dysbiotic bacteria
• Fewer proteases
• Less PAR2 activation

Diet changes the species. Species change the proteases. And proteases change the inflammation.

3. The epithelial cells in the colon's lining are replaced very rapidly, with the entire lining being replaced approximately every 3 to 5 days. That ensures that any cells containing "stuck on" PAR2 will be destroyed, and replaced by new cells every 3 to 5 days. Therefore, as the diet changes reduce the general inflammation level in the colon, the newly replaced cells will be less and less likely to be injected with PAR2, so that the inflammation level will eventually return to normal, and any pain associated with the inflammation will dissipate.

That said, the reason that MC and other IBD's are chronic, is because the healing process is corrupted. The first stage of the healing process is inflammation. With IBD's, the healing process is stuck on the first stage, because the inflammation is constantly being regenerated (with almost every meal). But once the diet is modified to remove the inflammatory foods, healing can become "unstuck" and proceed normally.

1. Lakemeyer, M., Latorre, R., Blazkova, K., Lomax, A. E., Bunnett, N. W., and Bogyo, M. (2025). A Bacteroides fragilis protease activates host PAR2 to induce intestinal pain and inflammation. Cell Host & Microbe, 33(10), pp 1686–1702. e11. Retrieved from https://www.cell.com/cell-host-microbe/abstract/

2. Teng, S. L., Latorre, R., Bhansali, D., and Bunnet, N. W. (2025). Nanomedicines targeting protease-activated receptor 2 in endosomes provide sustained analgesia. PNAS, 122(41). e2412687122 Retrieved from https://www.pnas.org/doi/10.1073/pnas.2412687122