You went away for two weeks, ate things you have not risked in years, and your gut behaved perfectly. Then you got home and it was back, sometimes before you had unpacked. That pattern is real, it is extremely common, and the internet's two standard explanations, "it's the stress" and "it's the food where you live", are both too simple to survive the details.
The single most useful clue is not what you ate abroad. It is how fast the symptoms returned. When someone describes normal bowel movements for fourteen days and then diarrhoea the morning after landing, having eaten one orange and a cup of tea, no dietary or microbial story can move that quickly. Something faster is doing the work.
This article takes the vacation effect apart properly: what actually changes when you travel, which of those changes has real evidence behind it, why the speed of the relapse matters more than anything on the plate, and how to run the experiment properly once you are home so you get an answer instead of another theory.
The short answer: four variables move together, and one of them moves in minutes
IBS is classified as a disorder of gut-brain interaction, a framework carried forward in the latest Rome update to the bowel disorder criteria (Corsetti 2026). That classification is not a polite way of saying "it is in your head". It means the symptoms arise from the interaction between what the gut is doing and how the nervous system reads and modulates it, and that both sides are legitimate targets.
That matters here, because the four things a holiday changes act on completely different timescales:
| What changed | How fast it can affect symptoms | Strength of evidence |
|---|---|---|
| Demands, attention and anticipation | Minutes | Strong, both experimental and clinical |
| Physical activity and walking | Hours to days | Moderate, with a randomised trial |
| Sleep and body-clock timing | A day or two | Moderate, mostly observational |
| Food composition and portions | Hours | Strong for fermentable carbohydrates, weak for most other food theories |
| Gut bacterial composition | Days | Demonstrated, but too slow to explain a same-day change |
Read that table next to your own experience and it usually answers the question on its own. If your symptoms took ten days to settle abroad and ten days to return, several explanations are in play. If they returned the evening you landed, the top row is doing most of the work.
The clue everyone misses: how fast it comes back
A recurring post in r/ibs describes two symptom-free weeks abroad, a flight home, an ordinary evening snack, and the worst diarrhoea in weeks the next morning (r/ibs thread). In the comments, several people describe the same thing on an even shorter fuse, including one who says it takes about ten minutes after walking through the door. These are descriptions of lived experience rather than data, but the timing is the interesting part, because it is testable against what we know about each candidate mechanism.
Gut bacteria are too slow. In a controlled feeding study, switching volunteers onto entirely animal-based or entirely plant-based diets did change gut microbial community structure quickly by microbiome standards, with changes detectable within days (David 2014). Days is fast for a microbiome. It is nowhere near fast enough to explain symptoms that return the same evening, especially when you have not yet eaten a full day of home food.
Accumulated additives are too slow and too vague. Any theory in which a substance builds up in your body over weeks of eating local food predicts a gradual return over weeks, not an overnight one.
Inflammation is not involved. In IBS there is no inflammatory lesion that could flare and settle. That is what separates IBS from Crohn's disease and ulcerative colitis, and it is why our Crohn's flare article has to answer a different question entirely.
Perception and motility are fast enough. Attention, anticipation and autonomic arousal change how much distension you notice, and how the bowel responds, on a scale of minutes. In a classic experiment, healthy volunteers had balloon distensions applied to the intestine under two conditions: paying attention, or distracted by a mental task. Perception scores were significantly higher during attention than during distraction, and the area over which people felt the sensation was larger, while intestinal compliance and reflex relaxation stayed unchanged (Accarino 1997). The gut was doing the same thing. The reading of it changed.
What a holiday actually removes, and it is not "stress" in general
Most articles stop at "you were less stressed". That answer is unsatisfying for a good reason: enormous numbers of people insist they are not stressed at home. The person who started the most-upvoted travel thread in r/ibs said exactly that, adding that they are effectively retired and have little to be stressed about (r/ibs thread). Another commenter pointed out that holidays with IBS can be considerably more stressful than staying home. Both are fair objections, and a good explanation has to survive them.
What travel removes is more specific than general stress:
- Fixed obligations at fixed times. The thing that makes urgency frightening is not the urgency, it is the meeting, the commute, the school run, the appointment you cannot leave.
- Toilet accounting. Many people with IBS run a continuous background calculation about bathroom access. On holiday that calculation often stops, paradoxically at the exact moment when bathroom access is worst. One person in the r/ibs travel thread described hyperventilating at the airport about finding toilets across Italy, then spending three weeks out in cities all day with no urgency at all.
- Role and identity load. Work, caregiving and household responsibility do not switch off because you feel calm about them.
This kind of gut-focused anxiety is measurable. The Visceral Sensitivity Index was developed and validated specifically to capture anxiety about gastrointestinal sensations and the situations in which they might occur, and performed well on reliability and predictive validity in 96 patients with IBS (Labus 2004). In a longitudinal study of 150 people with IBS followed through six to twelve months of usual treatment, improvement was strongly associated with gastrointestinal-specific anxiety, although in that analysis alexithymia rather than gut-specific anxiety was the factor that independently predicted outcome over time (Porcelli 2017). In people with panic disorder, those who also met criteria for IBS had higher anticipatory anxiety than those who did not (Sugaya 2013), which is a different population from most readers of this article but shows the anticipation link is not hand-waving.
Note what this framework predicts that the "relaxation" story does not. It predicts you can be objectively more stressed on holiday, sleep-deprived, jet-lagged, lost, and still feel better, because the specific demand that your gut was organised around is absent. Several people in these threads describe exactly that.
For the physiology of how stress signals reach the bowel, including the human experiment on intestinal permeability, our article on whether stress can cause an IBS flare covers it properly and this one will not repeat it.
"But I am genuinely not stressed at home"
There are two honest responses to this, and they point in different directions.
The first is that felt stress and registered stress are not the same measurement. In a human study, public speaking increased small intestinal permeability, and the effect was present only in the subgroup whose salivary cortisol actually rose. An anticipated-electric-shock protocol, which people found unpleasant but which did not raise cortisol, did not increase permeability (Vanuytsel 2014). What your body responded to was not what you would have listed as stressful.
The second response is more useful: if you are confident you are not stressed at home, stop trying to make stress the answer and look at the other three variables. Sleep timing, step count and meal structure are all concrete, all measurable, and all change dramatically on holiday. You do not need the psychological explanation to be true for the vacation effect to be real.
Your body clock moved, and your gut's timing moved with it
On holiday most people wake without an alarm, eat later, eat more slowly, and go to bed at a different hour. That is not a neutral change for the bowel.
Rotating shift work, which is the most extreme version of clock disruption, is associated with a higher prevalence of IBS. Among 399 nurses, rotating shift workers met Rome III criteria for IBS at 48% versus 31% of day-shift nurses, and the association held after correcting for age, gender and sleep quality (Nojkov 2010). This is cross-sectional, so it cannot tell you which came first, and it is one workplace population rather than the general public.
The microbial side has a mechanism too. Gut microbial communities in both mice and humans show daily oscillations driven substantially by feeding rhythms, and induced jet lag disrupted those oscillations in both species (Thaiss 2014). The outcomes measured in that work were metabolic rather than symptomatic, so it does not show that jet lag changes IBS symptoms. It shows the clock reaches the microbiome, which is a weaker but still relevant claim.
Sleep quality matters in a more directly measurable way. In a week of wrist actigraphy plus daily bowel diaries in 24 people with IBS and 26 healthy controls, the number of waking episodes during the night predicted worse abdominal pain and gastrointestinal distress the following day, though not stool pattern or bloating (Patel 2016). That is a small study, and mood partly explained the relationship, but it is one of the few that measured sleep objectively rather than asking people how they slept.
If your mornings are the worst part of your day at home and not on holiday, the mechanism is worth reading about separately in why IBS flares up in the morning, which covers the waking colonic response and the difference between waking naturally and waking to an alarm.
You walked fifteen thousand steps a day
This is the most underrated variable in the entire discussion, and it has better evidence behind it than almost any of the food theories.
Mild physical activity moves gas through the intestine faster. In eight healthy adults given a continuous jejunal gas infusion, gas retention was lower during intermittent pedalling than during rest, and the abdominal distension that developed at rest was significantly reduced by exercise (Dainese 2004). Eight people is a tiny study and they were healthy volunteers lying supine on a bike, not tourists walking round a city, so take the mechanism seriously and the numbers lightly.
For symptoms rather than mechanism, 102 people with IBS were randomised either to increase physical activity with physiotherapist guidance or to carry on as usual. The activity group's IBS Severity Scoring System score fell by a median of 51 points versus 5 points in the control group, a significant difference, and fewer people in the activity group got worse over the study (Johannesson 2011). A 2019 systematic review pooling 14 randomised trials and 683 patients across yoga, walking, Tai Ji, mountaineering and qigong concluded that exercise showed significant benefit but that the trials carried a strong risk of bias and no firm conclusion could be drawn (Zhou 2019). That is the honest position: probably helpful, not proven.
Several people in the r/FODMAPS Europe thread landed on this independently, describing six or more miles of walking a day and reasoning that faster transit means less time for fermentation (r/FODMAPS thread). That reasoning is roughly right, and it is one of the few holiday variables you can genuinely bring home.
Clairop logs meals, symptoms and stool in seconds, then looks for the foods your gut reacts to, including reactions that land days later.
The food really was different, but mostly not in the way the threads say
Some of the food differences people notice are real. Others are folk theory that has hardened into fact through repetition. It is worth separating them.
Bread is the one with an actual mechanism
If you ate bread and pastries abroad with no trouble and cannot touch them at home, the most plausible explanation is fructan content, which is driven heavily by how long the dough was fermented.
Start with what actually causes the symptoms. In a double-blind crossover challenge, 59 people on self-instituted gluten-free diets who did not have coeliac disease were given bars containing gluten, fructans or placebo. Overall symptom scores were highest after fructans, and there was no difference between gluten and placebo (Skodje 2018). For most people who feel bad after bread, the fermentable carbohydrate is the culprit, not the protein.
Fructan content in bread is not fixed. In a randomised double-blind crossover trial, 87 people with IBS ate low-FODMAP rye bread and regular rye bread for four weeks each. Flatulence, abdominal pain, cramps and stomach rumbling were all milder on the low-FODMAP bread, and breath hydrogen, a marker of colonic fermentation, was significantly lower. Notably, the overall IBS-SSS score and quality of life did not differ (Laatikainen 2016). A small SmartPill study in seven patients found roughly 40% lower breath hydrogen with the low-FODMAP bread but no statistically significant symptom difference (Pirkola 2018). A follow-up analysis found the two breads did not alter microbial diversity (Laatikainen 2019).
So the honest summary is: the measurable fermentation difference is solid, the symptom difference is real but modest and not present on every measure.
What drives the difference is time. Work on sourdough fermentation found that reaching low-FODMAP cutoff values required both a fermenting yeast and an extended dough fermentation of more than six hours, with a 24-hour cold ferment performing best (Wittwer 2024); this particular report is a preprint of a study later published in a food science journal, and it measured bread chemistry, not people. Industrial bread made on a rapid schedule has had less time for fructans to be broken down than a loaf proved overnight. That is a genuine, mechanistically coherent difference between bakeries, and it has nothing to do with which country you are in except insofar as baking traditions differ.
Our article on why bread makes IBS worse goes further into this.
Portion size, fat load and meal timing
Holiday meals are often earlier, longer, more leisurely and, in many places, smaller per course while larger in total. Fat load matters independently: in 61 people with IBS and 20 controls, a one-hour duodenal lipid infusion lowered colonic pressure thresholds for discomfort and pain significantly more in patients than controls, and widened the area over which sensation was referred (Simrén 2007). A fatty meal does not just sit heavily. It measurably turns up colonic sensitivity for a while afterwards.
Fructose is worth a mention because of how often high-fructose corn syrup comes up in these threads. Fructose malabsorption is genuinely common in IBS: in a retrospective series of patients who had both tests, fructose and fructan malabsorption on hydrogen breath testing were associated with each other (Sia 2024), and a multicentre prospective study examined how positive glucose, lactose and fructose breath tests related to symptom severity and quality of life (Loo 2025). What none of this establishes is that one national sweetener is the reason your holiday went well. Sucrose and high-fructose corn syrup differ modestly in free fructose, and nobody has run the comparison in people with IBS.
The detail that argues against a pure food explanation
Read the threads carefully and you will notice something awkward for the food theory: people report drinking considerably more alcohol on holiday and feeling better anyway. In a month-long daily-diary study of women with IBS and healthy controls, binge drinking, defined as four or more drinks in a day, was associated with worse gastrointestinal symptoms the next day in the IBS group specifically, including diarrhoea, nausea and stomach pain, while moderate and light drinking showed weak or no association (Reding 2013). This was women aged 18 to 48 and it is observational, so it shows association rather than cause.
If your alcohol intake went up and your symptoms went down, something else was more than compensating. That is a data point about your own case, and it is the kind of internal contradiction most articles about this topic skip past.
What about the additives everyone blames?
This comes up in every thread, usually in strong terms. It deserves a careful answer rather than either dismissal or amplification.
What is true: countries do permit different food additives. Some flour treatment agents and colourings used in one jurisdiction are not authorised in another. This is a genuine regulatory difference and people are not imagining it.
What I could not verify this run: I was not able to open the primary regulatory texts, because both the United States electronic Code of Federal Regulations and the relevant agency pages blocked automated access during this research. So this article does not quote a specific permitted concentration or a specific ban date for any additive, and you should treat any page that does without a primary citation with some caution. Regulatory status also changes, sometimes at state or national level within a single year.
What does not appear to exist: evidence connecting those additives to IBS symptoms in people. A Europe PMC search in September 2026 for potassium bromate or azodicarbonamide together with irritable bowel syndrome returned zero results, and a search for glyphosate together with irritable bowel syndrome also returned zero. That is not proof of safety and it is not proof of harm. It means the study that would settle the argument has not been published, and everyone in the comment section arguing about it is arguing past the evidence in both directions.
The cleanest counter-argument to the food-supply theory comes from the threads themselves. In the r/FODMAPS Europe thread, a European commenter who moved to Asia and then to North America reported their gut was worse in North America. In the r/ibs travel thread, an American living in France reported that their bowels are usually great when they visit the United States. A theory in which one country's food supply is the cause has to explain why the effect reverses depending on which direction you are travelling. The theory in which travel itself is the active ingredient does not have that problem.
The counterpoint nobody posts about: plenty of people get worse
If you are about to travel rather than looking back on a trip, our guide to travelling with IBS-D covers the practical side: the infection risk that outlasts the trip, toilet access, and what is worth packing.
The keyword for this article assumes IBS improves on holiday. For a large number of people it does the opposite, and the evidence base leans that way harder than the threads suggest.
- Travel constipation is common and appears in the threads themselves, with people describing bowels that shut down completely while away and then open up dramatically on return.
- Travellers' diarrhoea carries a real long-term risk. A meta-analysis of six studies found the pooled relative risk of post-infectious IBS after travellers' diarrhoea was 3.35 (95% CI 2.22 to 5.05), with overall post-infectious IBS incidence of 5.4% in people who had travellers' diarrhoea versus 1.4% in those who did not (Schwille-Kiuntke 2015). Self-reported rather than laboratory-confirmed travellers' diarrhoea produced a higher relative risk, which the authors flag as a limitation of relying on recall.
- Bathroom access abroad is objectively worse, not better, for anyone whose symptoms include urgency.
So why do the "my IBS vanished abroad" posts dominate? Because they are surprising and worth writing. Nobody posts "I had a bad stomach on holiday, as usual". This is straightforward selection in what gets written down, and it is the single biggest reason the internet's picture of this phenomenon is lopsided. Functional bowel disorders are common worldwide, not a feature of any one country's food supply: in the Rome Foundation Global Epidemiology Study across 26 countries, 33.2% of people met Rome IV criteria for some functional bowel disorder (Tornkvist 2026).
Were the two weeks really better, or did you catch a good stretch?
This is worth asking before you redesign your life around the answer.
IBS fluctuates substantially on its own, which is why our article on why IBS comes and goes exists at all. Two weeks is a small sample of days. If you have a good fortnight roughly every couple of months anyway, the probability that one lands on a holiday is not small, and you will remember the holiday one.
The trial literature makes the same point from a different direction. In a meta-analysis of herbal medicine trials in IBS, the placebo response rate across 1,151 patients in placebo arms was 37% (Huang 2024), and a network meta-analysis of 45 double-blind trials in 5,174 patients found that placebo response on quality-of-life outcomes varied substantially by the form the placebo took (Wang 2025). People in IBS trials who receive nothing active frequently improve, and part of that is the natural waxing and waning of the condition being measured at a moment when it happened to be bad.
None of this means your holiday was imaginary. It means one holiday is one data point, and two or three trips showing the same pattern is much stronger evidence than one.
A worked example: taking one trip apart
Here is how the decomposition looks in practice. Imagine a two-week trip to southern Europe, symptoms gone, symptoms back the day after landing.
| Variable | On holiday | At home | Can you bring it home? | Worth testing? |
|---|---|---|---|---|
| Daily steps | 14,000 | 3,500 | Partly | Yes, first |
| Wake-up | No alarm, 8:30am | Alarm, 6:15am | Sometimes | Yes |
| Largest meal | 2pm, eaten slowly | 8:30pm, eaten fast | Often yes | Yes |
| Bread | Long-fermented, local bakery | Supermarket sliced | Yes | Yes |
| Alcohol | Higher | Lower | Not the direction you want | No |
| Coffee | Small, after food | Large, on an empty stomach | Yes | Yes |
| Toilet vigilance | Low | High | Hard, but treatable | Yes |
| Work obligations | None | Full | No | Not directly |
The point of laying it out like this is that it immediately kills the single-cause instinct. Almost nobody's trip differs on one line. And the right-hand column shows why a diary is worth keeping: four of those rows are cheap to test and reversible, and the two that are not testable, alcohol and work, are not the ones you would want to replicate anyway.
How to run the experiment properly once you are home
The mistake almost everyone makes is changing five things at once in the week after a trip, feeling better for a few days, and then losing the thread. The structure that works is boring and slow.
- Establish a baseline first. Two weeks of ordinary home life, logging stool form on the Bristol scale, pain, urgency and bloating once or twice a day. Without a baseline you cannot tell a change from a fluctuation. If you are unsure what to record, our guide to keeping a food diary for IBS covers the mechanics.
- Rank your variables by cost. Steps and meal timing are free. Changing your bread supply is cheap. Replumbing your kitchen is not. Do them in that order regardless of which theory you find most appealing.
- Change one thing, and hold it for at least two weeks. Most useful changes do not declare themselves in three days, and three days is short enough that normal fluctuation will fool you either way.
- Do not change anything else during that window, including the thing you changed last time if it did not help. Put it back.
- Re-test whatever seems to work. If raising your step count helps, drop it back down for a fortnight and see if symptoms return. An effect that survives being removed and reinstated is worth believing. The logic here is the same challenge and rechallenge design covered in how to find out what triggers your IBS.
- Write down what you expected before each block. Expectation is a real contributor in IBS, and recording it in advance at least lets you notice when the result matched your hope suspiciously well.
Tracking timestamped meals and symptoms in one place is exactly what Clairop is built for, because the whole point of this exercise is spotting delay patterns you cannot hold in your head.
One caution on interpretation: fermentable carbohydrates stack, so a food can sit safely under your threshold on a low-load day and over it on a high-load day. That is why "it was fine abroad" is not evidence the food is safe in isolation. We cover this in why safe foods sometimes trigger IBS and in the FODMAP stacking examples.
What tends to help, ranked honestly by evidence
If the pattern really does point at the gut-brain side, there are treatments with trial evidence behind them. None of them is a cure, and none of them works for everyone.
Gut-directed hypnotherapy. In the IMAGINE trial, 354 people with IBS in the Netherlands were randomised to individual hypnotherapy, group hypnotherapy or group educational supportive therapy. At three months, adequate relief was reported by 40.8% of the individual hypnotherapy group, 33.2% of the group hypnotherapy group and 16.7% of controls; at twelve months the figures were 40.8%, 49.5% and 22.6%. Hypnotherapy beat the control condition at both time points, and group delivery was non-inferior to individual (Flik 2019). The trial reports no funding. A more recent pilot of nurse-led online group hypnotherapy in 51 patients found 53% met the responder threshold of a 50-point IBS-SSS reduction, sustained at six months, but it was a single-arm pilot with no control group (Lövdahl 2026).
Cognitive behavioural therapy, particularly with interoceptive exposure. In a Japanese trial, 114 people with drug-refractory IBS were randomised to ten weeks of group CBT with interoceptive exposure or to a waiting list. The CBT group improved by 115.8 points on the IBS Symptom Severity Score versus 29.7 in the waiting-list group (Kikuchi 2022). This trial was open-label with a waiting-list comparator, which inflates apparent effects for any psychological intervention, and the authors say so. Interoceptive exposure is relevant here because it targets precisely the toilet-vigilance loop that a holiday interrupts.
Guidelines back this route. The American College of Gastroenterology suggests gut-directed psychotherapy to treat global IBS symptoms (Lacy 2021), and the British Society of Gastroenterology guideline, which reclassified IBS as a disorder of gut-brain interaction, reviews psychological therapies alongside dietary and pharmacological options (Vasant 2021).
Digital delivery is being tested and the results are not a slam dunk. A four-arm randomised trial in 642 adults compared internet-delivered general patient education alone against the same plus a CBT module, a FODMAP module, or both, with dietitian messaging available to all groups (Thuen 2026). The design is worth knowing about if you are considering an app-based programme, because it asks the right question: what do the added modules contribute over education alone?
Physical activity, covered above, is the cheapest intervention with randomised evidence (Johannesson 2011).
Do not start, stop or change any medication or supplement based on this article. These are conversations to have with your GP or gastroenterologist.
Myths about the vacation effect
"It proves my IBS is psychological." No. It shows that gut-brain pathways contribute, which is true of IBS by definition and is not the same as the symptoms being imagined. Distension perception changed measurably with attention in healthy volunteers with no IBS at all (Accarino 1997).
"It proves the food where I live is poisoning me." The effect reverses direction depending on which way people travel, which a country-specific food theory cannot accommodate. The bread mechanism is real; the blanket version is not supported.
"It must be the tap water at home." If unfamiliar water caused gut symptoms, travellers would be worse abroad, which is the actual epidemiological pattern (Schwille-Kiuntke 2015). If you have a specific reason to suspect your water supply, that is a question for your water provider and your doctor, not for a symptom diary.
"It must be gluten, since European bread is fine." Under double-blind conditions, gluten performed no differently from placebo, while fructans produced significantly higher symptom scores (Skodje 2018). The mechanism is fermentation and fructan content, not the protein.
"The microbiome reset while I was away." Microbial composition does shift with diet, but over days (David 2014), and the low-FODMAP and regular rye bread comparison found no change in microbial diversity at all over four weeks (Laatikainen 2019). Neither timescale fits a symptom change that reverses in an afternoon.
"If I moved abroad, I would be fine." Nothing in this article supports that. The people who describe moving rather than visiting tell more mixed stories, and functional bowel disorders are common across all 26 countries in the Rome Foundation global study (Tornkvist 2026).
When to see a doctor
Everything above assumes IBS that has already been diagnosed by a clinician. If nobody has assessed you, the pattern described here is not a substitute for that assessment, and a good holiday does not rule anything out.
See a doctor promptly if you have any of the following, whether or not they started around a trip:
- Blood in your stool, or black tarry stools.
- Diarrhoea persisting more than about two weeks after travel. This is the one most specific to this article. Post-travel diarrhoea can have treatable infectious causes, including parasitic ones, and should be investigated rather than assumed to be IBS. A confirmed gut infection also more than triples the risk of developing post-infectious IBS (Schwille-Kiuntke 2015), so it is worth documenting even once it settles.
- Unexplained weight loss or loss of appetite.
- Fever alongside gut symptoms.
- Symptoms that wake you from sleep, which are covered in IBS waking me up at night.
- New bowel symptoms starting after the age of 50.
- A family history of bowel cancer, coeliac disease or inflammatory bowel disease.
- Anaemia, or being told your iron is low.
If you have Crohn's disease or ulcerative colitis rather than IBS, this article is the wrong frame. Symptoms improving abroad does not tell you anything about inflammation, and symptom scores and objective inflammation can move independently in both directions. Contact your IBD team about any change in bleeding, stool frequency or new pain.
The honest bottom line
The vacation effect is real, widely reported, and almost never caused by one thing. Four variables move together, and they act on different timescales, which is why the speed of your relapse is more informative than anything you ate.
If symptoms came back the same day you got home, the fastest-acting mechanisms are the most likely candidates, and those are the gut-brain ones: attention, anticipation, and the constant low-level accounting that many people with IBS run about toilets and obligations. If they came back gradually over a week or two, food composition, meal timing, activity and sleep all become plausible and are worth testing one at a time.
What the evidence does not support is the confident version of either popular story. "It was just stress" ignores the walking, the sleep and the bread. "It is the food supply where I live" cannot explain why the effect reverses when people travel the other way, and the specific additives blamed most often have not been tested against IBS symptoms in a single published study I could find.
The useful move is not to pick a side. It is to bring home the two or three holiday variables you can actually reproduce, change them one at a time, and give each one long enough to prove itself.
