Gut Guide · Antibiotics and the microbiome

The gut after antibiotics: what can support the rebuild and what slows it down

The basic pattern returns within weeks. Individual residents stay away longer. And of all things, the most careful study on this question arrives at a result that puts the common recommendation in doubt.

SJ
Shukri Jarmoukli · Physician · Focus of practice: integrative and functional medicine · ViveCura Berlin
Recovery times with their measure Suez 2018 in context The guideline in its own words 27 sources with DOI
ViveCura BlogGut Guide › The gut after antibiotics

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Why I am writing this

The most common question after a course of antibiotics is which product rebuilds the gut. The better question is which of two questions you are actually asking. Symptoms during the course and diversity afterwards are not the same thing. The studies give different answers to each, and that is exactly why the guides contradict one another.

The infection is gone, the belly feels different

The last tablet sits in an empty blister. The fever has been gone for days, the cough as well. The matter is, in principle, settled.

Only your belly has not noticed yet.

It makes sounds it did not make before. The bowel movement is softer than usual, or it does not come at all. After eating there is a tight feeling. And somewhere at the back of your mind sits the sentence you picked up between two appointments: after antibiotics you have to rebuild the gut.

Many people know this pattern. In my consultation it comes up almost weekly, usually with the same question in tow. Which product should I take.

First a sentence that stands above everything else. Antibiotics save lives. This text does not judge any medical prescription and at no point advises stopping, shortening or refusing a prescribed antibiotic. A course that has been started is finished as it was prescribed. Everything written here comes afterwards.

And one more sentence about the term itself. Gut restoration is not a defined medical procedure. There is no guideline for it, no fixed sequence and no endpoint that is examined anywhere. The term describes an intention, not a method. I use it here because you searched for it, and because you should know which data sit behind the word and which do not.

First things first

Red flags: these signs belong in a medical assessment, not in self treatment

  • blood in the stool, or black, tarry stool
  • unintended weight loss
  • fever
  • night time symptoms that wake you
  • vomiting or difficulty swallowing
  • a new, persistent change in bowel habit from around 45 to 50 years of age
  • anaemia
  • bowel cancer or inflammatory bowel disease in the family

These signs are not a case for self experiments and no reason to postpone a recommended examination. They belong in a medical consultation promptly. After a course of antibiotics one more point comes on top, which I cover further down: diarrhoea that does not stop after the last tablet, or that starts only weeks later.

What you will find here

  • What antibiotics measurably change in the microbiome, on four levels
  • Why the time frames run from four weeks to two years and are all correct
  • The finding by Suez and colleagues, in full and with its limits
  • Why meta-analyses support probiotics and the German guideline still gives no recommendation
  • Two questions that get mixed up constantly, placed side by side
  • The quiet brakes: acid blockers, repeated courses, alcohol, lack of sleep
  • What can support the rebuild, and where the analogy begins
  • Clostridioides difficile and the signs where waiting is not an option
  • Why there is no test that proves a gut has been rebuilt
  • The bigger frame: life saving and still often without indication
RCT / Meta randomised or pooled Human cohort, case control, survey In vivo animal model, not tested in humans In vitro cell culture, far from everyday life

And now to the question you are actually here for. What is going on down there.

What antibiotics actually change in the microbiome

Imagine a meadow with a few hundred plant species growing on it. Some in large patches, many only in single spots. An antibiotic is not a lawnmower that cuts everything to the same height. It is more like a very selective herbicide that hits certain species hard and others barely at all.

What happens afterwards can be described on four levels, and these four levels recover at different speeds. That is the reason for the contradictory time frames online.

Level one: diversity

Diversity means how many species are there and how evenly they are distributed. It drops quickly after an antibiotic and usually comes back. But not immediately, and not in everyone to the same degree.

Intervention study, n=12 The reference study for time frames

An international team around Albert Palleja gave twelve healthy men a combination of three reserve antibiotics for four days, namely meropenem, gentamicin and vancomycin. Their stool was then examined over six months with shotgun metagenomics, so not only for the species list but also for the resistome, the entirety of resistance genes.

Directly after the course, enterobacteria and other pathobionts bloomed, while bifidobacteria and butyrate producers were thinned out. After about 1.5 months the composition was close to the starting state again. Nine species, however, that had been detectable in all twelve participants beforehand, stayed below the detection limit in most of them after 180 days. Species carrying beta lactam resistance genes were positively selected during and after the intervention.

For you this means: the basic pattern returns within weeks. Individual residents stay away longer, some across the entire observation period of the studies. The authors themselves explicitly call the microbiome of young healthy adults resilient, and that part of the finding belongs here just as much as the other.

Palleja A, Mikkelsen KH, Forslund SK et al. Nat Microbiol. 2018;3(11):1255-1265. PMID: 30349083 · DOI: 10.1038/s41564-018-0257-9 [Cohort, n=12]

Level two: composition

Diversity can come back without the same species coming back. Two meadows with the same number of plant species can look completely different.

Longitudinal, n=3 A third shifted, and nobody notices

Les Dethlefsen and colleagues followed three healthy people before and after a course of ciprofloxacin, with more than 7,000 full length sequences and more than 900,000 pyrosequencing reads. In total they identified 3,300 to 5,700 taxa.

Ciprofloxacin influenced the abundance of about one third of these taxa and lowered species richness, diversity and evenness. Four weeks after the end of treatment the composition in all three closely resembled the previous state again, yet several taxa did not recover within six months. One sub clause in the abstract is remarkable: all participants reported normal bowel function throughout.

For you this means: a third of the taxa shifted, and the belly feels normal. Symptoms and microbiome change can come apart. Freedom from symptoms does not mean that nothing happened. And symptoms do not automatically mean that your microbiome is the problem.

Dethlefsen L, Huse S, Sogin ML, Relman DA. PLoS Biol. 2008;6(11):e280. PMID: 19018661 · DOI: 10.1371/journal.pbio.0060280 [Cohort, n=3]

The same group looked more closely three years later, over ten months with two courses of ciprofloxacin in between. Per person 52 to 56 stool samples, more than 1.7 million sequences in total. The effect set in within 3 to 4 days of starting. About a week after the end of each course the return began, but it often stayed incomplete. In the end the composition had stabilised in all three, yet it was changed compared with the starting state. The authors describe this as a possible switch into an alternative stable state.

The second observation matters: the reaction differed between the three people, even between the two courses in the same person. There is no standard course. That is uncomfortable and honest.

Reframe

Return is not the same as restoration. When a guide writes that the gut flora is back after six weeks, it means the similarity of the overall pattern. It does not mean that every single species is back. Putting both into one sentence creates either false reassurance or unnecessary worry.

For everyday life this is good news. Your gut is not a clockwork with a missing cog. It is an ecosystem in which different residents can take over similar tasks. That is why digestion often works again long before the species list looks the same.

Level three: individual species that do not come back

The longest documented time span comes from a Swedish study, and it is the reason why some texts speak of years.

Controlled, n=8 Two years later, still different

Cecilia Jernberg and colleagues gave four people clindamycin for seven days, while four others served as a control group. Over two years, stool samples were analysed at nine time points.

The clonal diversity of the Bacteroides isolates dropped sharply, highly resistant clones persisted long term, and the Bacteroides community did not return to its original composition across the entire two year period. In addition there was a sustained increase of specific resistance genes in the stool DNA. In the control group, by contrast, the fluctuations over time were small.

For you this means: after a single week of a particularly invasive antibiotic, something was still measurably different two years later. Eight people are a very small number, and clindamycin is a special case, more on that below. The finding still works as a counterweight to any statement that recovery is finished after six weeks.

Jernberg C, Löfmark S, Edlund C, Jansson JK. ISME J. 2007;1(1):56-66. PMID: 18043614 · DOI: 10.1038/ismej.2007.3 [Cohort, n=8]

The methodologically cleanest study in this block is a different one, and it supports the same point with considerably more people.

RCT, n=66 The mouth comes back, the gut needs longer

Egija Zaura and colleagues randomised 66 healthy adults in the United Kingdom and Sweden to four different antibiotics or placebo: clindamycin, ciprofloxacin, amoxicillin and minocycline. Stool and saliva were examined at baseline, directly afterwards and after 1, 2, 4 and 12 months.

The salivary microbiome proved considerably more robust and recovered quickly. The faecal microbiome was strongly altered by most of the antibiotics, in such a way that health associated butyrate producers stayed strongly underrepresented for months. Genes for antibiotic resistance were enriched.

For you this means: two mucous membranes, the same tablet, two completely different courses. Butyrate is the main energy source of the large bowel lining. Why that is more than a footnote is set out in the article on L-glutamine, butyrate and the gut lining.

Zaura E, Brandt BW, Teixeira de Mattos MJ et al. mBio. 2015;6(6):e01693-15. PMID: 26556275 · DOI: 10.1128/mBio.01693-15 [RCT, n=66]

Level four: the resistance genes

This is the half of the story that practically never appears in guides. An antibiotic does not only change who lives in the gut. It also changes which tools these residents carry with them.

Resistance genes are blueprints with which bacteria can render an antibiotic harmless or pump it out of the cell. They can be passed on between bacteria, including between different species. Taking an antibiotic can give exactly these carriers an advantage. In Palleja, species with beta lactam resistance genes were positively selected, in Jernberg the genes stayed elevated for two years, in Zaura they were enriched.

This is no reason for a guilty conscience and no argument against a necessary course. It is the reason why careful use of antibiotics is a medical goal.

The core of this section

Four time frames, four different measures

3 to 4 days
until the effect sets in, measured as a drop in diversity and a shift in compositionDethlefsen & Relman 2011, three people over ten months
about 4 weeks
until the overall composition closely resembles the previous state againDethlefsen 2008, three people after ciprofloxacin
about 1.5 months
until the composition is close to the starting value again, after four days with three reserve antibiotics at oncePalleja 2018, twelve healthy men
180 days
and nine species present in everyone beforehand are still missing in most of themPalleja 2018, the same group
up to 2 years
until the Bacteroides community after one week of clindamycin is still not the old one, with resistance genes elevated across the whole periodJernberg 2007, eight people

These numbers only appear to contradict each other. Each of them measures something different. Anyone who wants to name a single number has to say what was measured, otherwise exactly the confusion arises that you find online.

And now you know why the question how long does this take has no single answer. It has five, and each of them is right for its own measure.

The finding that puts the common recommendation in doubt

If you have read this far, one conclusion suggests itself. If antibiotics thin out diversity, then you simply top it up. You give bacteria back. That sounds so logical that hardly anyone questions it.

In 2018 an Israeli group tested exactly that. And the result is uncomfortable.

Clinical trial in humans Mouse model In vitro part The core finding of this article

Jotham Suez, Niv Zmora and colleagues at the Weizmann Institute compared three routes after a course of antibiotics: spontaneous recovery without any addition, a multi strain probiotic, and an autologous faecal transplant, meaning a person's own gut flora, frozen before the course and given back afterwards. What is decisive about the design: not only stool was examined but, by endoscopy, the mucosa itself, plus the host transcriptome, meaning which genes the gut cells read. The same setup ran in parallel in mice, along with a laboratory part in cell culture.

First, against expectation: after antibiotics the probiotic colonised the human mucosa even better than in the normal state. Second, the core finding: compared with spontaneous recovery, the probiotic led to a markedly delayed and persistently incomplete return of the person's own microbiome, in stool and in mucosa, and likewise to a delayed return of the host transcriptome towards the starting state. Third: under the autologous faecal transplant the system returned almost fully within days in this study. That is a result from a single study and not a promise for an individual person. Fourth, in the laboratory: soluble factors released by Lactobacillus contributed to the inhibition of the person's own microbiome.

For you this means: topping up from the outside can slow down the return of what is your own. The authors write in the abstract themselves that a possible benefit of probiotics after antibiotics may be offset by a compromised recovery of the gut mucosa.

Suez J, Zmora N, Zilberman-Schapira G et al. Cell. 2018;174(6):1406-1423.e16. PMID: 30193113 · DOI: 10.1016/j.cell.2018.08.047 [Clinical Trial, human] [In vivo, mouse] [In vitro]

Before this turns into a campaign against probiotics, four limitations belong with it.

What this study does not show

Four limitations that belong with it

First, the sample size is not publicly verifiable. The abstract names none, and the full text sits behind a paywall. That is why this article states no participant number. What can be verified is the design, the three routes compared, the invasive sampling and the classification as a clinical trial. That the probiotic mixture contained eleven strains is documented through the sister study from the same group.

Second, it measures a different target than the diarrhoea studies. What was measured is the restoration of the microbiome, not the number of days with diarrhoea. Turning this into probiotics are harmful has swapped two endpoints.

Third, it is a single study. A very careful one, and methodologically unusually deep, but a single one. A finding only becomes robust once an independent group has repeated it. That has not happened so far.

Fourth, the autologous faecal transplant is not an everyday option. It was a study arm, not an offer. In Germany, faecal microbiota transfer is according to the German guideline so far only available within individual treatment attempts, and nobody routinely freezes their stool before a planned course of antibiotics. For now, no practical route follows from the finding.

The sister study from the same programme also explains why people react so differently to the same product.

Clinical trial, humans and mice Why the same product does two things in two people

The same group examined healthy people and mice in the normal state, again with invasive sampling from the mucosa. They received either a combination of eleven probiotic strains or placebo.

The probiotics survived the passage through stomach and gut alive. Whether they actually colonised the mucosa, however, was specific to the person, to the gut segment and to the strain, and could be predicted from baseline features of host and microbiome. In colonised mice they met a pronounced colonisation resistance, in germ free mice they did not. Decisive for practice: whether colonisation had taken place could not be seen in the stool.

For you this means two things. If a product changed something for your colleague and not for you, neither of you is doing anything wrong. And a stool test cannot answer this question, because stool does not reflect colonisation of the mucosa. What a stool test can and cannot do is set out in the article on stool testing, PCR and dysbiosis diagnostics.

Zmora N, Zilberman-Schapira G, Suez J et al. Cell. 2018;174(6):1388-1405.e21. PMID: 30193112 · DOI: 10.1016/j.cell.2018.08.041 [Clinical Trial, human] [In vivo, mouse]

This leaves two camps facing each other. One says probiotics belong after every antibiotic. The other says they do nothing. Both cite real studies, and both are talking about different things.

The central distinction

Two questions that get mixed up constantly

Question A: will I get diarrhoea during the course?
What is measured
whether a defined symptom occurs, within a fixed time window, mostly during and shortly after the course
Evidence
good. 63 randomised trials with 11,811 people, plus separate meta-analyses on individually named strains
Answer
a named strain can lower the risk. How strongly depends on the baseline risk and therefore on the situation
Who decides
medically, according to risk factors, not across the board
Question B: will my own diversity come back afterwards?
What is measured
how quickly and how completely a person's own microbiome returns to the starting state in stool and mucosa
Evidence
thin. At its core a single, very careful study, without independent replication
Answer
there the multi strain probiotic delayed the return, while the person's own flora, given back, sped it up
Who decides
so far nobody. For this question there is no robust recommendation yet

The most dangerous mistake would be to turn question B into a blanket ban on probiotics. The second most dangerous would be to keep quiet about question B because it is uncomfortable. Both columns stand side by side, because they measure different things and both of them are real.

The other side: where probiotics have good data

Now column A. And it is strong.

Antibiotic associated diarrhoea is not a marginal phenomenon. The German guideline gives a frequency of about 10 percent under parenteral antibiotic therapy, and more than 75 percent of these cases are not infectious. For exactly this problem there is a large landscape of studies.

Meta-analysis, 63 RCTs, n=11,811 The large JAMA meta-analysis

Susanne Hempel and colleagues searched twelve databases without language restriction and included 82 randomised trials on probiotics in antibiotic associated diarrhoea.

The pooled analysis of 63 of these trials with 11,811 participants produced a relative risk of 0.58, with a confidence interval of 0.50 to 0.68 and a number needed to treat of 13. Heterogeneity was substantial, the measure I squared was 54 percent. The authors stress explicitly that the strains were poorly documented and that the evidence is not sufficient to say for which people, which antibiotics and which products the effect holds.

For you this means: statistically about one in thirteen people treated benefits by not getting diarrhoea. That is a real effect. It says nothing about whether your diversity comes back faster afterwards, because that was not the question asked.

Hempel S, Newberry SJ, Maher AR et al. JAMA. 2012;307(18):1959-1969. PMID: 22570464 · DOI: 10.1001/jama.2012.3507 [Meta-analysis, k=82, n=11,811]

The picture becomes considerably sharper when you look at a single named organism instead of the category.

Meta-analysis, 21 RCTs, n=4,780 Saccharomyces boulardii in detail

Hania Szajewska and Marek Kołodziej updated a meta-analysis from 2005 and included 21 randomised trials with 4,780 participants, 16 of them new, with a GRADE rating of the evidence quality.

Overall, the risk of antibiotic associated diarrhoea fell from 18.7 to 8.5 percent, relative risk 0.47, number needed to treat 10. In children from 20.9 to 8.8 percent, in adults from 17.4 to 8.2 percent. For Clostridioides difficile associated diarrhoea the risk reduction was statistically meaningful only in children, not in adults.

For you this means: it depends on the specific organism, not on the word probiotic on the packaging. And it depends on the question you ask. Good numbers for ordinary antibiotic diarrhoea, and not for Clostridioides difficile in adults. Who this yeast is expressly not suitable for is in the safety box further down.

Szajewska H, Kołodziej M. Aliment Pharmacol Ther. 2015;42(7):793-801. PMID: 26216624 · DOI: 10.1111/apt.13344 [Meta-analysis, k=21, n=4,780]

And now comes the number that explains why the German guideline still gives no recommendation.

Cochrane, 39 trials, n=9,955 The benefit hangs on the baseline risk

Joshua Goldenberg and colleagues evaluated 39 randomised trials with 9,955 participants for the Cochrane Collaboration, on the prevention of Clostridioides difficile associated diarrhoea.

The main analysis across 31 trials with 8,672 people produced 1.5 percent under probiotic against 4.0 percent under placebo, relative risk 0.40, number needed to treat 42, certainty of evidence moderate. The subgroup analysis is decisive: at a baseline risk of 0 to 2 and of 3 to 5 percent there was no difference. Only at a baseline risk above 5 percent was there a large risk reduction, namely 3.1 against 11.6 percent, number needed to treat 12. Detection of the organism itself in stool was not reduced.

For you this means: the benefit is not wrong, it is tied to a precondition. Where the event is rare, the effect disappears. Where it is common, it is large. That is exactly why a guideline cannot give a blanket recommendation without naming the target group.

Goldenberg JZ, Yap C, Lytvyn L et al. Cochrane Database Syst Rev. 2017;12(12):CD006095. PMID: 29257353 · DOI: 10.1002/14651858.CD006095.pub4 [Systematic Review, Cochrane, k=39, n=9,955]

How far this carries is shown by the largest single trial in this field. It found nothing, and that is an important result.

RCT, n=2,981 PLACIDE, the trial without an effect

Stephen Allen and colleagues screened 17,420 inpatients aged 65 and over in the United Kingdom who received at least one antibiotic, and randomised 2,981 of them double blind to a multi strain preparation of lactobacilli and bifidobacteria with a total of 6 times 10 to the power of 10 organisms per day over 21 days, or to an identical looking placebo.

Antibiotic associated diarrhoea within eight weeks: 10.8 percent under probiotic against 10.4 percent under placebo, relative risk 1.04, p equals 0.71. Clostridioides difficile diarrhoea within twelve weeks: 0.8 against 1.2 percent, relative risk 0.71, p equals 0.35. The detailed report additionally shows that duration and severity of diarrhoea, common gastrointestinal symptoms, quality of life and health care costs did not differ either.

For you this means: in a large, cleanly conducted trial in a specific population, no effect was visible. The dose figure comes from this trial and is purely literature here, not a recommendation. It shows that the question does not hang on the amount.

Allen SJ, Wareham K, Wang D et al. Lancet. 2013;382(9900):1249-1257. PMID: 23932219 · DOI: 10.1016/S0140-6736(13)61218-0 [RCT, n=2,981]
Safety

Who probiotics are not suitable for

One sentence belongs here that the Cochrane authors write themselves and that most guides leave out. They call short term use safe and effective, and expressly in people who are not immunocompromised and not severely debilitated. That is not a formality. The very group in which the benefit appears at all in this analysis is at the same time the group at highest risk.

With a strongly weakened immune system, under chemotherapy, after a transplant or with a central venous catheter, bloodstream infections caused by the administered yeasts and bacteria have been described, in individual cases with a severe course. Yeast preparations containing Saccharomyces boulardii are therefore not suitable for severely ill and immunocompromised people, nor for people carrying a central line. The same caution applies to preparations with lactic acid bacteria in that situation.

If you or a relative belong to this group, a probiotic is not something for your own shopping basket. That decision belongs in the hands of the treating doctor, who knows the situation.

And independently of that: unwanted effects are described in otherwise healthy people too. In the Cochrane trials the most common were abdominal cramping, nausea, fever, soft stools, flatulence and taste disturbance, and in both groups. Anyone taking a preparation who notices new or stronger symptoms should discuss that medically rather than increase the amount.

What the guidelines make of this

And here it becomes interesting. The guidelines say neither the one nor the other. They say a third thing.

“A recommendation for the prophylactic use of probiotics cannot be given.”

DGVS, S2k guideline Gastrointestinal Infections, recommendation 3.12, modified 2023, open recommendation, strong consensus, translated from the German original

The decisive part is not in this sentence but in the reasoning behind it. The guideline sets out that the Cochrane benefit only appears from a frequency of at least 5 percent in the treated population. And that such a frequency is reached in Germany almost only in one high risk group, namely people with acute leukaemia or after allogeneic stem cell transplantation. On top of that, it remains unclear which probiotic would be meant, because the meta-analyses pool different products.

That is not a rejection. That is arithmetic.

Two other professional societies reach slightly different conclusions from the same evidence. The European society for paediatric gastroenterology formulates recommendations only where at least two randomised trials exist for a strain named with its strain designation. If risk factors are present in children, for example antibiotic class, duration of treatment, age, hospital care or previous episodes, it names Lactobacillus rhamnosus GG or Saccharomyces boulardii, each with moderate evidence quality and a strong recommendation. Without risk factors, it does not. American gastroenterology likewise decides by indication and strain, and names the low certainty of evidence explicitly.

Nuance

Why gastroenterology is reserved here, and why that is not a contradiction

A guideline answers a very precise question: does this product prevent a defined event in this group of people. For that question it needs an event that occurs often enough. Otherwise every effect disappears in the noise, see PLACIDE. It also needs a defined product, and that is exactly what is missing, because probiotic is not a substance but a category.

The functional view asks a different question: does diversity come back, and how quickly. For that question there are hardly any hard endpoints, but with the study by Suez there is a finding that puts the obvious answer in doubt.

The most honest sentence in this article is therefore: the guidelines are not silent out of ignorance. They are silent because the question many people ask has no robust study answer so far. That is a good reason for restraint, and it deserves respect rather than contradiction.

What form and strain even mean is set out in the article on probiotics in spore form versus capsule form. Here it stays at two sentences, because this article answers a different question.

And now you know why you find two camps online, both pointing at real studies. They asked different questions.

What slows the rebuild, often without you noticing

The more interesting part of the question is rarely what you take in addition. It is what works against recovery at the same time. While you are busy with a product, several brakes are often running in the background. Some of them are even on a prescription.

The second course of antibiotics

The study by Dethlefsen and Relman over ten months included two courses of ciprofloxacin. After the second one, recovery was not the same as after the first. A meadow that is treated twice in the same year looks different afterwards than one that is treated once.

For the very long time frame there is a large observational study that I place carefully.

Cohort, n=16,642 Decades instead of weeks

Yin Cao and colleagues analysed 16,642 women aged 60 and over from the Nurses' Health Study who had had at least one colonoscopy by 2010. Antibiotic use at ages 20 to 39 and 40 to 59 was recorded, as well as the most recent use.

Among 1,195 adenoma cases, an increasing duration of use at ages 20 to 39 and 40 to 59 was associated with a higher adenoma risk. At least two months of antibiotics between 20 and 39 gave an odds ratio of 1.36, between 40 and 59 one of 1.69. Use in the four years before the survey was not associated with adenoma risk.

For you this means: an association, not a cause. The reason for the antibiotic course can itself be the risk factor, which is called confounding by indication. I do not cite this study to create fear, but for one calm sentence. Repeated courses over decades leave more behind than a single course, and that is one of the arguments for careful use. It is not an argument for turning down a necessary prescription.

Cao Y, Wu K, Mehta R et al. Gut. 2018;67(4):672-678. PMID: 28377387 · DOI: 10.1136/gutjnl-2016-313413 [Cohort, n=16,642]

The strongest single brake sits on a prescription

This is the point where many guides stop and where it actually starts to become interesting.

Cohort, n=1,815 Acid blockers change more than antibiotics

Floris Imhann and colleagues sequenced the stool microbiome of 1,815 people from three Dutch cohorts and compared people with and without proton pump inhibitors, first per cohort and then pooled in a meta-analysis.

211 participants were taking an acid blocker at the time of sampling. Taking one was associated with a meaningfully lower Shannon diversity and with changes in 20 percent of the bacterial taxa. In users, several oral bacteria were overrepresented in stool, among them the genus Rothia. The sentence the study hangs on: at population level the effects of acid blockers are more pronounced than those of antibiotics or other commonly used medicines.

For you this means: anyone taking an acid blocker in addition after a course of antibiotics has two factors at the same time. These are observational data, not causality. For the link with Clostridioides difficile the German guideline states explicitly that a causal relationship is currently not established, because acid blockers are often used in people who carry other risk factors anyway.

Imhann F, Bonder MJ, Vich Vila A et al. Gut. 2016;65(5):740-748. PMID: 26657899 · DOI: 10.1136/gutjnl-2015-310376 [Cohort, n=1,815]

Why stomach acid matters for the gut at all can be said in one sentence. It is the first barrier between what you eat and what arrives in the small intestine. If there is less acid up top, more can arrive further down that does not belong there.

From clinical practice

Stomach acid first

In my practice, with gut topics I first ask whether there is enough acid up top, before I think about anything else. Digestive enzymes come after that question with me, not before it. That is an order that comes from clinical work, not a ranking proven by studies, and I name it as such. What follows from it in an individual case is something I decide in the consultation, not in a text. Taking a preparation on suspicion is expressly not what is meant.

More on this in the article on low stomach acid and betaine HCl. If it is more about heartburn, the article on heartburn and acid blockers belongs beside it. Both topics need their own depth.

Important

No changes to prescribed medication on your own

Nothing in this section means that you should stop, reduce or pause a prescribed acid blocker. The same applies to laxatives, to immunosuppressive therapies and, of course, to antibiotics. An acid blocker is often prescribed for very good reasons, for example to protect the stomach lining under other medicines.

The right action is a different one: bring the question to your next medical appointment. Whether a long term prescription still fits is a medical decision, and every adjustment belongs in medical hands.

Alcohol, a one sided diet, lack of sleep, stress

On alcohol there is a study with mucosal biopsies. Ece Mutlu and colleagues examined colonic biopsies from 48 people with alcohol dependence and 18 healthy controls. A subgroup showed an altered colonic microbiota, with fewer Bacteroidetes and more Proteobacteria, in part linked with high endotoxin levels in the blood. The connectedness of the community was reduced, even after longer abstinence.

Two limitations definitely belong with this: it was about alcohol dependence, not about a glass of wine in the evening. And only a subgroup was affected. A number for moderate consumption cannot be derived from it. As a direction the finding still holds.

A very one sided diet is the second brake, and the most common one. Anyone living on toast, rusks and bananas for two weeks after an infection feeds a very small selection of residents. For a few days that is fine. As a permanent state it takes the basis away from exactly those species that are trying to come back.

Lack of sleep and stress belong on this list as well, without me pulling in a single study for it here. For the link between sleep and the microbiome I have gathered the evidence in the article on sleep and the gut microbiome. For the connection through the nervous system the same applies in the article on the gut brain axis and vagus stimulation. Both are mechanistically well founded and thinner in human evidence than the guides suggest. That is exactly how it belongs named.

The quiet brakes at a glance

  • Another course of antibiotics shortly afterwards. Sometimes unavoidable. Where it is avoidable, the conversation about it is worth having.
  • An acid blocker running alongside. Not to be stopped on your own. Discuss medically whether it is still needed.
  • A very one sided diet over weeks. Sensible as light food for days, counterproductive as a permanent state.
  • Regular alcohol. The data come from dependence, the direction is clear enough anyway.
  • Chronic lack of sleep and constant stress. Mechanistically well founded, thinner in human evidence than it is often presented.
  • Impatience. The time axis lies at weeks to months. Anyone who tries the next product after ten days is only measuring their own restlessness.

And now you know why the question what do I take is often the smaller half. The bigger one is what is working against it at the same time.

What can support the rebuild

Now the part you were probably waiting for. It begins with a limitation that applies to the whole section.

None of the studies in this section was carried out in people after a course of antibiotics. All of them are analogies. That is no reason to leave them out, but a reason to label them. Where the label [Analogy, not tested in people after antibiotics] appears, that is exactly what I mean.

Substrate variety instead of a single number

Bacteria do not eat fibre in general. They eat particular sugar chains, and different species eat different ones. A meadow with thirty plant species needs more than one fertiliser. Variety on the plate is therefore the more plausible target than a number of grams. How robust the famous number 30 is can be found in the article on the fibre myths. Here the finding of a single randomised trial is enough, because it is unexpectedly fine grained.

RCT, n=36 Fermented against high fibre, compared directly

Hannah Wastyk and colleagues randomised 36 healthy adults over 17 weeks to two dietary patterns: high in fibre or rich in fermented foods, 18 per arm, with extensive immune profiling.

The high fibre diet increased the glycan degrading enzymes encoded in the microbiome, yet left the diversity of the community stable. In the fibre arm, three different immunological trajectories appeared, which were linked to the baseline diversity. The diet with fermented foods, by contrast, increased diversity steadily, and several inflammatory markers went down. One point belongs with it that many summaries leave out: the prespecified primary endpoint of the trial, a composite cytokine response score, did not change in either group. The findings on diversity and on the inflammatory markers are therefore secondary results. They are interesting and they are not proof.

For you this means: fibre alone did not increase diversity in this trial, fermented foods did. That is finer than the common rule of thumb and still not a free pass. The participants were healthy and had no course of antibiotics behind them. [Analogy, not tested in people after antibiotics]

Wastyk HC, Fragiadakis GK, Perelman D et al. Cell. 2021;184(16):4137-4153.e14. PMID: 34256014 · DOI: 10.1016/j.cell.2021.06.019 [RCT, n=36]

In practice this does not mean: eat two kilos of sauerkraut now. It means: in the trial cited it was the fermented foods group in which the described changes appeared, so yoghurt, kefir, sauerkraut, kimchi and miso. For the time after a course of antibiotics this has not been tested, and no effect on your recovery can be promised from it. It is the route with the least uncertainty and not the route with proof of effect. Variety on the plate beats a single number.

Two limits belong with this. In pregnancy, unpasteurised fermented and raw milk products do not belong on the plate because of listeria, and pasteurised versions are the way here. And anyone who reacts sensitively to histamine often tolerates matured fermented products poorly.

The convenient way out that is not one

At this point many texts add the sentence that you should simply take prebiotics instead of probiotics. So not bacteria, but their food. It sounds elegant. It is less well studied than it sounds.

Animal study, mouse The prebiotic delayed things as well

Chunhui Tao and colleagues gave male BALB/c mice an antibiotic cocktail for seven days. Their microbiome then recovered either spontaneously or with the addition of 5 percent inulin type fructans over 14 days.

The inulin delayed the recovery from the antibiotic induced colitis compared with spontaneous recovery. Neither with nor without inulin did the community return to the baseline composition at genus level. Inulin did increase individual beneficial bacteria and the butyrate level, but at the same time it led to selective blooms of individual opportunistic organisms. The return of the immunoglobulin genes was also delayed under inulin. The authors conclude that caution is warranted when trying to counter an antibiotic induced dysbiosis with prebiotics.

For you this means: no recommendation against prebiotics in humans follows from a mouse model. What does follow is that the idea of taking the food instead of the bacteria is not as clean as it sounds. The only study that has tested this question specifically after antibiotics is this one, and its result is uncomfortable. [Animal study, no transfer to humans]

Tao C, Zeng W, Zhang Q et al. J Appl Microbiol. 2020;130(3):634-649. PMID: 32813896 · DOI: 10.1111/jam.14827 [In vivo, mouse]

What prebiotics and resistant starch actually feed in the normal case, and where their strengths lie, is a topic of its own. In the situation directly after a course of antibiotics I name the gap instead of filling it. That is the more honest answer.

Movement

Jacob Allen and colleagues had 32 previously inactive adults, 18 of them lean and 14 with obesity, train under supervision three times a week for six weeks. Six weeks without training followed, and diet was controlled before each sample.

In the lean participants the short chain fatty acids in stool rose, in those with obesity they did not. The practically most important finding comes at the end: the changes largely receded once the training stopped. Two honest sentences follow from this. Movement can shift the microbiome measurably, but apparently only while it is happening. And the effect is not the same in everyone. [Analogy, not tested in people after antibiotics]

Sleep and time

Sleep belongs on this list because it is the condition for almost everything else. I give no numbers, because for the question after antibiotics I found no verifiable human study that I could cite in good conscience.

And then time. The least popular point, and probably the most important. The time axis here lies at weeks to months, not at days. An ecosystem that is sorting itself out again is hard to hurry along. Anyone who tries the next product after ten days out of dissatisfaction has never let the first step run its course.

Reframe

Substrate beats product. The question which product is the worst documented question in this entire field. The question what lands on my plate over the next eight weeks is the best documented one, even where the evidence rests on analogies.

This is not a rejection of products. It is an order. Variety on the plate, fermented foods, movement, sleep and patience are the ground. Whether something additional makes sense on top of that is an individual question, and one I ask in the consultation rather than answer in a blog article.

If symptoms persist for weeks, something other than plain recovery can be behind them. Bacterial overgrowth in the small intestine is one of the possibilities that can be examined medically, and there is the article on SIBO for that. Overgrowth with yeasts is also often discussed, and what needs saying about it is in the article on Candida in the gut. And coeliac disease can hide behind persistent diarrhoea too, particularly when the symptoms are first noticed after an infection.

Two further possibilities I name here expressly, because they are often noticed late. Microscopic colitis causes watery diarrhoea without blood, often over weeks, and it cannot be seen with the naked eye during a colonoscopy. It shows up only in the tissue samples taken during it. If a colonoscopy is coming up for you and the diarrhoea persists, that is a good point to raise beforehand, and there is the article on microscopic colitis for it. The second is a disturbed bile acid cycle, which can likewise cause watery diarrhoea and responds to something entirely different, and there is more on that in the article on bile and bile acids. Both belong in a medical assessment and not with preparations from the internet.

Important

If coeliac disease is suspected: assess first, then change the diet

Anyone switching to a gluten free diet before the diagnostic work up can make the diagnosis impossible. The antibodies in the blood and the changes in the tissue sample recede under a gluten free diet, and then the test comes back unremarkable although coeliac disease is present. Anyone who then has to switch back to gluten in order to be able to test at all has lost weeks, and often gained symptoms along the way.

The order is therefore: first the assessment, then the change of diet. Gluten stays on the plate until the diagnostics are done, and this decision belongs in a medical conversation. What is examined is set out in the article on recognising coeliac disease. Why gluten can be a topic even without coeliac disease is a different question, written up in the article on gluten and gliadin without coeliac disease.

And now you know why the most honest advice in this section sounds boring. It is boring because it is documented.

Clostridioides difficile: the case that belongs in medical hands

Up to here it was about nuances. Now it is about a clear line.

There is one situation after antibiotics in which self experiments are the wrong route and delay can do harm. It has a name.

Mechanism

How a thinned out meadow turns into an infection

  1. Clostridioides difficile is a spore forming bacterium. Its spores survive conditions under which other bacteria die off, including most antibiotics.
  2. In a densely populated gut it has little chance. The existing community occupies the places, uses up the nutrients and can change the bile acids so that the spores hardly germinate.
  3. An antibiotic can thin out this community. With that, several of these protective mechanisms can fall away at the same time.
  4. Now the spores can germinate and multiply. The bacteria can form toxins that attack the lining of the large bowel.
  5. The consequence can be watery diarrhoea, often with abdominal pain and fever, in severe cases with a pronounced inflammation of the large bowel.

This is also why the study by van Nood fits here so well: what is missing is not a single strain, but a functioning community.

How strongly an antibiotic is linked with this infection differs considerably between the classes.

Meta-analysis, 7 observational studies An antibiotic is not simply an antibiotic

Kevin Brown and colleagues searched EMBASE and PubMed without time or language restriction for studies on the link between antibiotic exposure and a community acquired Clostridioides difficile infection. Of 465 articles screened, seven met the criteria.

Compared with no antibiotic exposure, the pooled odds ratios were 16.80 for clindamycin, 5.50 for fluoroquinolones, 5.68 for cephalosporins, monobactams and carbapenems together, 2.71 for penicillins, 2.65 for macrolides and 1.81 for sulfonamides and trimethoprim. For tetracyclines there was no effect. The German guideline lists the same orders of magnitude.

For you this means: if you feel worse after an antibiotic than your neighbour did after hers, part of the answer lies here. But no wish list follows from it. Which antibiotic is used is decided by the prescribing physician according to the infection, the pathogen and the resistance situation, not according to the microbiome.

Brown KA, Khanafer N, Daneman N, Fisman DN. Antimicrob Agents Chemother. 2013;57(5):2326-2332. PMID: 23478961 · DOI: 10.1128/AAC.02176-12 [Meta-analysis, k=7]

One note that goes beyond the microbiome and belongs here. All the substances named are prescription only, and the choice is made by the prescribing doctor according to pathogen and resistance pattern, not according to the microbiome. For fluoroquinolones, which include ciprofloxacin, the European authorities restricted use in 2019. The reason is rare but partly long lasting and sometimes not reversible problems affecting tendons, muscles, joints and the nervous system, along with a signal for bulges of the main artery. They should therefore no longer be used for mild infections where an alternative is available.

If you notice tendon pain or abnormal sensations during or after such a course, that belongs in a prompt medical assessment. With sudden severe pain in chest, abdomen or back, call the emergency number 112 and do not wait. That is not a reason to stop a started course on your own, but a reason to discuss it medically.

From the German guideline

Who carries an increased risk

Antibiotic therapy
currently or within the last three months
Previous infection
a Clostridioides difficile infection within the last twelve months
Age
over 65 years
Stay
hospital stay currently or within the last three months, or living in a communal facility
After transplantation
status after stem cell or organ transplantation
Pre-existing conditions
inflammatory bowel disease, chronic internal medical conditions

If an inflammatory bowel disease is known in your case, you will find the integrative context in the article on Crohn's disease and colitis. For this article it counts as a risk factor, no more.

The standard has changed recently. In its current version the German guideline names fidaxomicin as the preferred first line treatment, a prescription only antibiotic directed specifically at Clostridioides difficile which, on the available data, affects the rest of the gut flora less strongly than the earlier standard agents. Like any antibiotic it can have side effects, among them nausea, vomiting and abdominal pain, and it is not suitable where a hypersensitivity is known. Which agent fits in an individual case is decided by the treating doctor according to severity, history and accompanying conditions. Doses I deliberately do not give here.

With repeated relapses a faecal microbiota transfer can be considered, in Germany so far as an individual treatment attempt. Where the diagnosis is suspected or confirmed, stopping proton pump inhibitors should also be considered. Each of these points is a medical decision, not a self treatment measure.

How much a complete community can achieve is shown by the study that gave the procedure its breakthrough.

RCT, n=43 What a whole community can achieve

Els van Nood and colleagues randomised people with recurrent Clostridioides difficile infection to three arms: a short course of vancomycin plus bowel lavage plus infusion of a donor stool solution through a nasoduodenal tube, standard vancomycin over 14 days, or standard vancomycin plus bowel lavage.

The trial was stopped after an interim analysis. Of 16 patients in the infusion group, 13, so 81 percent, were free of symptoms after the first infusion, two more after a second infusion with stool from a different donor. Under vancomycin alone it was 4 of 13, under vancomycin plus bowel lavage 3 of 13. After the infusion, bacterial diversity in stool rose to a level similar to that of the healthy donors.

For you this means two things. First, this finding makes the study by Suez plausible: a matching, complete community can achieve what individual strains cannot. Second, faecal transplantation is a medical procedure with a clear indication, not a wellness offer and not a route for the time after an ordinary antibiotic. ViveCura does not offer this procedure. I describe the study here solely in order to explain why a complete community can do something that individual strains cannot.

van Nood E, Vrieze A, Nieuwdorp M et al. N Engl J Med. 2013;368(5):407-415. PMID: 23323867 · DOI: 10.1056/NEJMoa1205037 [RCT, n=43]
Do not wait

When diarrhoea after antibiotics belongs in a medical examination

  • diarrhoea that does not stop once the antibiotic is finished
  • diarrhoea that begins only weeks after the course
  • diarrhoea with fever, severe abdominal pain or blood
  • a course of antibiotics within the last three months together with new diarrhoea
  • a previous Clostridioides difficile infection within the last twelve months
  • age over 65 years, a hospital stay in the last three months, or living in a care facility
  • status after stem cell or organ transplantation, inflammatory bowel disease or chronic internal medical conditions

Immediately, and not at the next working day, according to the criteria of the guideline translated into everyday language, these belong on the list: severe dehydration, circulatory weakness, very severe abdominal pain, neurological abnormalities and persistently bloody diarrhoea. These are reasons for an assessment in hospital. With clouded consciousness, circulatory collapse or rapidly worsening condition, call the emergency number 112 and do not wait for an appointment.

In infants and small children the window is much shorter than in adults, because they dehydrate faster. Persistent diarrhoea, repeated vomiting, markedly fewer wet nappies, a dry mouth or striking tiredness belong promptly in a paediatric consultation.

And one point that is often forgotten: with severe or persistent diarrhoea the effectiveness of oral contraception can be impaired. Anyone using it should check the package leaflet or clarify it medically and use an additional method during that time.

Here a probiotic is not the answer, and a stool test from the internet is not either. The answer is a medical examination with targeted diagnostics. If the symptoms remain afterwards and nothing threatening is found, that is not a dead end but the beginning of a different search. There is the article on IBS and the search for causes for that, because part of these courses begins after an infection.

And now you know where the line between self care and diagnostics lies. It is not blurred. It is sharp.

The bigger question that does not belong in your belly

There is a sentence that is constantly misused in this field, and I would like to write it down properly.

Antibiotics are one of the most effective inventions in medicine. Pneumonia, blood poisoning, meningitis, a severe wound infection: in all of these situations an antibiotic decides whether someone survives. That is the starting point, and nothing that follows changes it.

At the same time there are numbers showing that they are used more often than guidelines would consider appropriate. These numbers describe a system, not a single person and not a single prescription.

Analysis, n=184,032 visits The American stocktaking

Katherine Fleming-Dutra and colleagues analysed two national American surveys of ambulatory care from 2010 and 2011, 184,032 visits in total. Using national guidelines and regional differences in prescribing behaviour, they estimated for each diagnosis what share of the prescriptions was appropriate.

12.6 percent of the visits ended with an antibiotic prescription. Extrapolated, this gave 506 prescriptions per 1,000 inhabitants per year, of which an estimated 353 were appropriate. For acute respiratory conditions together, 221 prescriptions per 1,000 inhabitants stood against an estimated 111 appropriate ones.

For you this means: a model calculation against guidelines, not a review of individual cases, and these are American data. For your own prescription exactly nothing follows from it. For the overall picture, quite a lot does.

Fleming-Dutra KE, Hersh AL, Shapiro DJ et al. JAMA. 2016;315(17):1864-1873. PMID: 27139059 · DOI: 10.1001/jama.2016.4151 [Cohort, n=184,032 visits]

So that the article does not argue with American numbers alone, here is the European addition, in which German practices also took part.

Survey, n=4,982, 18 countries Europe, and a surprising side finding

Alike van der Velden and colleagues prospectively documented 4,982 primary care consultations for sore throat or lower respiratory tract infection in 18 European countries, including illness characteristics and the clinicians' own confidence in their decision.

The prescribing shares varied considerably, from under 20 percent in four countries to over 40 percent in six countries. The use of point of care tests also varied strongly, from 0 percent in three countries to over 65 percent in Denmark and Norway. Prescribing followed illness severity, comorbidity, age, fever and country, but not whether a rapid test had been done. In almost 90 percent of the consultations the clinicians were confident in their decision.

For you this means: the difference is not down to a lack of care by individuals. It is down to habits, expectations and systems in which the same situation is decided differently in one country than in the one next door. Even a test result changed little about the decision.

van der Velden AW, van de Pol AC, Bongard E et al. BJGP Open. 2022;6(2):BJGPO.2021.0212. PMID: 34920989 · DOI: 10.3399/BJGPO.2021.0212 [Cohort, n=4,982, 18 countries]
The sentence that matters here

This is no argument against a prescribed antibiotic. It is an argument for a conversation at the next infection. So for the question: what speaks for it in my case, and what speaks against it. You ask this question before the prescription, not afterwards, and you ask it together.

In practice this conversation takes pressure off both sides. Saying that you would also go home content without a prescription, provided that is medically defensible, changes the situation. And anyone with a clear indication gets their antibiotic and takes it in full.

What you can realistically expect

That leaves the question you probably came with. When is this over. The honest answer has four parts.

3 to 4 days until the effect on diversity and composition sets in
4 to 6 weeks until the overall pattern closely resembles the starting state again
180 days and individual species are still missing in most people
2 years longest documented time span for individual markers after one week of clindamycin

First, what comes back. The basic pattern, diversity as a number, function. In young healthy adults usually within about six weeks.

Second, what often does not come back. Individual species. In the study of twelve men there were nine of them missing in most participants after half a year. Whether that matters for you personally has not been studied so far.

Third, why you do not feel it. In Dethlefsen a third of the taxa were shifted, and all participants reported normal bowel function. Symptoms and microbiome can be decoupled, in both directions. If your belly causes symptoms after a course of antibiotics, the cause is not automatically the species list. It can also lie in motility, in the gut lining, in what you ate while ill, or in something else entirely.

Fourth, why there is no test for it. There is no blood value and no validated stool test that proves a microbiome has been rebuilt. Even the accepted definition for it is missing. And the sister study to the Suez work shows that stool does not even reveal whether a probiotic has colonised the mucosa. Which questions a stool test can answer is set out in the article on stool testing and dysbiosis diagnostics.

If after a course of antibiotics you want to sort out not just a single topic but the whole picture, you will find the frame in the article on the gut reset and holistic gut treatment. It orders the building blocks that are only touched on here.

To take away

The question is not whether you should do something for your gut after antibiotics. The question is which of the two questions you are answering right now. Symptoms during the course have a good study basis and a clear responsibility. Diversity afterwards has a thin study basis and an uncomfortable core finding. Separating the two leads to calmer decisions and saves a lot of products.

Frequently asked questions

How long does it take for the gut flora to recover after antibiotics?

That depends on what is being measured. In a study of twelve healthy men the composition was close to the starting value again after about 1.5 months. In another study it resembled the previous state again as early as four weeks after the end of treatment. Nine species that had been detectable in all twelve beforehand were missing in most of them after 180 days. And after one week of clindamycin the Bacteroides community was still not the old one two years later. A rough return within weeks, a fine imprint over months to years.

Does the gut flora come back completely after antibiotics?

The basic pattern usually does, individual residents often do not. The authors of the study of twelve men explicitly call the microbiome of young healthy adults resilient. At the same time, in several studies individual species stayed below the detection limit for months or years, and resistance genes stayed elevated. Complete in the sense of identical is rarely documented. Functionally unremarkable, by contrast, is the normal case.

Do probiotics after antibiotics make sense or not?

That depends on which question you mean. For preventing diarrhoea during a course of antibiotics there are good randomised data. For restoring your own diversity afterwards, the most careful study shows the opposite: a multi strain probiotic delayed the return of the person's own microbiome there. Both findings stand side by side, because they measure different things. Anyone who wants to decide should therefore clarify the goal first, ideally in a medical conversation. Important with it: with a weakened immune system, a severe underlying illness, under chemotherapy, after a transplant or with a central venous catheter, probiotics are not a self decision, because bloodstream infections caused by the administered organisms have been described in that situation.

Should I take a probiotic during or only after the course of antibiotics?

The meta-analyses on diarrhoea prevention mostly tested probiotics alongside the course of antibiotics, not in the time afterwards. The study on restoration after the course found an unfavourable result for exactly that time afterwards. No schedule and no time of day follows from this. What follows is the question of whether this is about symptoms during the course or about diversity afterwards. That question belongs before any purchase.

Which probiotic is the best after antibiotics?

This question has no product answer. Guidelines tie their recommendations to individual strains named with their strain designation, and not to the category probiotic. European paediatric gastroenterology names Lactobacillus rhamnosus GG and Saccharomyces boulardii, and only when risk factors are present. Meta-analyses, by contrast, pool products that are not biologically the same. A good average therefore says little about one particular pack.

Why does the German guideline not recommend probiotics routinely?

The S2k guideline of the DGVS writes, on preventing a Clostridioides difficile infection: “A recommendation for the prophylactic use of probiotics cannot be given.” The reasoning in the background text is arithmetic, not a verdict on probiotics. The benefit from the Cochrane review only appears from a baseline risk above 5 percent, and in Germany that risk is reached almost only by people with acute leukaemia or after allogeneic stem cell transplantation. On top of that it remains open which product would be meant.

What is an autologous faecal transplant, and can I have it done?

Here a person's own gut flora is frozen before a course of antibiotics and given back afterwards. In the study by Suez and colleagues the person's own microbiome returned almost fully within days by this route. That is a result from a single study and not a promise for an individual person. It is a study procedure. In Germany, faecal microbiota transfer is according to the guideline so far only available within individual treatment attempts, and freezing your own stool before a planned course is not on offer outside studies. So for now no practical route follows from the finding.

Are prebiotics or resistant starch the better choice after antibiotics?

The only study that has tested prebiotics specifically after a course of antibiotics is a mouse model. Inulin type fructans delayed recovery there compared with spontaneous recovery and promoted individual opportunistic organisms. For humans, neither a yes nor a no can be derived from it. The honest answer to this question is a gap in the research. Substrate variety through real food remains the route with the least uncertainty.

How long is diarrhoea after an antibiotic normal, and when does it belong in a medical assessment?

Under parenteral antibiotic therapy the frequency of antibiotic associated diarrhoea is about 10 percent according to the German guideline, and more than 75 percent of these cases are not infectious. It usually settles after the end of the course. Diarrhoea belongs in a medical assessment if it does not stop after the last tablet, if it starts only weeks later, or if it comes with fever, severe abdominal pain or blood. A course of antibiotics in the last three months plus new diarrhoea is also a reason for an examination. This is not a case for self experiments with products.

What is Clostridioides difficile, and how do I recognise it?

Clostridioides difficile is a bacterium whose toxins can trigger diarrhoea and inflammation of the large bowel. It gets its chance when the rest of the gut flora has been thinned out after a course of antibiotics. Typical signs are watery diarrhoea, abdominal pain and fever, often during or in the weeks after the course. According to the German guideline, increased risk is carried among others by people over 65 years, after a hospital stay, after stem cell or organ transplantation and with inflammatory bowel disease. Any suspicion belongs in a medical examination and not in self treatment.

Is yoghurt or kefir enough, or do I need a supplement?

Fermented foods are well studied, though not in the situation after a course of antibiotics. In a randomised trial over 17 weeks in healthy adults, a diet with fermented foods increased microbiome diversity steadily, and several inflammatory markers went down, while the high fibre arm did not increase diversity. The prespecified primary endpoint, a composite cytokine response score, did not change in either group. Transferring that to the time after antibiotics is an analogy, and no effect on your recovery can be promised from it. As an everyday route it is the one with the least uncertainty. In pregnancy, unpasteurised fermented and raw milk products are not part of it because of listeria.

Can acid blockers slow the rebuild after antibiotics?

In a cohort of 1,815 people, taking proton pump inhibitors was associated with lower diversity and with changes in 20 percent of the taxa, at population level more pronounced than the effect of antibiotics. These are observational data, not causality, and the German guideline stresses that explicitly. One sentence therefore matters: a prescribed acid blocker is not stopped on your own. Whether a prescription still fits belongs in a medical conversation, and every change belongs in medical hands.

Is there a test that shows me whether my gut has been rebuilt?

No. There is no blood value and no validated stool test that proves a microbiome has been rebuilt. The sister study to the Suez work even shows that stool does not reveal whether a probiotic has colonised the gut lining at all. A stool test can answer certain questions. This one is not among them.

I have had several courses of antibiotics in recent years. Is the damage permanent?

Seriously, this can neither be played down nor dramatised. After four days of reserve antibiotics, nine previously present species were missing in most people after 180 days, and after one week of clindamycin the Bacteroides community was still not the old one after two years. An observational study of 16,642 women found a higher rate of bowel adenomas with longer antibiotic use between the ages of 20 and 59, without a cause following from it. That is an argument for careful use of antibiotics, not an argument against a necessary prescription.

Where this topic connects to the rest of the body

The gut after a course of antibiotics does not stand on its own. It hangs on what lands on the plate, on sleep, on the nervous system and on the question of how well nutrients are taken up while the lining is busy.

SJ

Shukri Jarmoukli

Physician · Focus of practice: integrative and functional medicine · ViveCura Berlin

I work in my private practice at the intersection of conventional medicine, functional medicine and Clinical Psychoneuroimmunology. With gut topics I am less interested in which product is currently being recommended than in which question is actually still open before the next step.

On this topic I am more reserved than you might expect from an integrative practice. For the return of diversity after antibiotics there is no product with convincing data, and the most careful study on it even points in the other direction. This article does not replace medical advice. It should help you ask better questions at your next appointment.

ViveCura, Privatpraxis Shukri Jarmoukli, Skalitzer Straße 137, 10999 Berlin

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  12. Allen SJ, Wareham K, Wang D et al. Lactobacilli and bifidobacteria in the prevention of antibiotic-associated diarrhoea and Clostridium difficile diarrhoea in older inpatients (PLACIDE): a randomised, double-blind, placebo-controlled, multicentre trial. Lancet. 2013;382(9900):1249-1257. PMID: 23932219 · DOI: 10.1016/S0140-6736(13)61218-0 [RCT, n=2,981]
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Transparency on the evidence: where the data are thin
  1. The sample size of the core study is not in this article. The abstract by Suez and colleagues names none, and the full text is not freely accessible. Design, procedure and results are verified, a participant number is not. Estimating it would be sloppy, which is why it is missing.
  2. The core finding has not been independently replicated. It comes from a single, very careful study. Until another group confirms or refutes it, it remains a strong signal and not a proof.
  3. Prebiotics after antibiotics rest on a mouse model. Neither for nor against can anything be derived from it for humans. The article names the gap instead of filling it.
  4. Diet and movement are analogies. Neither the study on fermented foods nor the one on endurance training was carried out in people after a course of antibiotics. The transfer is plausible and not tested.
  5. The link between acid blockers and the microbiome is observational. The German guideline states explicitly that a causal relationship is currently not established, because acid blockers are often used in people who carry further risk factors.
  6. The link between antibiotics and later adenoma risk is an association. The study is observational and was carried out in women, and the reason for the antibiotic course can itself be the risk factor.
  7. Alcohol was studied in dependence, not in moderate consumption. Only a subgroup was affected on top of that. A number for a glass of wine cannot be derived from it.
  8. On sleep and the microbiome this article deliberately cites no single study. For the specific question after a course of antibiotics, no verifiable human study could be pinned down cleanly. The point therefore stands as a direction and is linked.
  9. The numbers on inappropriate prescriptions are model calculations. They compare observed prescribing behaviour with guidelines and regional differences. They do not examine any individual case, and part of the data comes from the United States.
  10. Two guideline documents are available without an abstract. The American papers on the role of probiotics are therefore described only in their structure and not cited with individual recommendation sentences. Only the German guideline, whose full text was checked, is quoted verbatim.
  11. There is no validated test for a gut that has been rebuilt. Even the accepted definition is missing. Every statement about an endpoint of recovery is therefore an approximation.
  12. What deliberately does not appear here. No dosing recommendation, no rebuild plan with week numbers, no product recommendation and no advice to change, reduce or stop a prescribed medication. Study figures on dosing appear purely as literature. From no section does it follow that a recommended assessment should be postponed or replaced. What I describe from my consultation is marked as an observation and is not a study result.

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