What to avoid: antibiotics, PPIs, ultra-processed foods

Sometimes the most important thing is what we DON'T do. Unnecessary antibiotics, needless acid suppressants and ultra-processed foods all undermine the freshly engrafted gut flora. This chapter teaches you to recognise and avoid the three main traps.

Antibiotics — the biggest risk

Antibiotics are the most important trigger of C. difficile infection. The logic is simple: an antibiotic does not discriminate, it destroys the disease-causing and the beneficial bacteria at the same time. When the protective gut flora is thinned out, C. difficile gets free room to overgrow. It was precisely this process that created your original infection, and it is precisely this that can trigger a relapse too — especially now, when the transplanted flora is still only taking root.

This does not mean you may never take antibiotics again. There will be situations — a severe bacterial infection — when they really are necessary. The goal is that you don't receive antibiotics needlessly: for a viral cold or flu, for example, they are of no use, because those are not bacteria. If any doctor wants to prescribe an antibiotic, always mention that you have been through C. difficile infection and are on an FMT course — this is important information that can influence the decision and the type of agent chosen.

As for the DiffBiome course: if you do need an antibiotic for some reason, the basic rule is that the antibiotic must be finished at least 48 hours before starting DiffBiome, otherwise the antibiotic would destroy the freshly delivered flora too. Always coordinate this with your treating physician.

The acid suppressant (PPI) — the silent risk

The proton pump inhibitor — PPI for short — is the most common acid-suppressing medication (they often end in "-prazole": omeprazole, pantoprazole and the like). Many people take them for heartburn or reflux, sometimes for years, without reconsidering whether they are still really needed.

Why does this matter for C. difficile? Stomach acid is one of your body's natural lines of defence: it destroys most of the swallowed pathogens before they reach the gut. If you persistently suppress acid production, this line of defence weakens, and unwanted bacteria can settle more easily — research has linked long-term PPI use with a higher C. difficile risk.

The important message: never stop this medication on your own, because some people genuinely need it (for example with ulcers or severe reflux). But it is worth discussing with your treating physician: is taking it still really justified, could the dose perhaps be reduced, or could it be replaced with lifestyle steps? It often turns out that an acid suppressant started long ago is no longer needed.

Ultra-processed foods — the everyday risk

The third trap lies in eating. Ultra-processed foods^[G] are those heavily industrially transformed products that contain many additives, emulsifiers, refined sugar and little fibre — think of packaged sweets, sugary soft drinks, fast food, the many brightly packaged snacks. These give exactly the opposite of what your engrafting gut flora needs.

Your gut flora, you see, lives on fibre and varied plant matter. Ultra-processed foods, by contrast, are low in fibre and, in return, full of additives (certain emulsifiers, for example) that, according to research, can disturb the protective layer of the gut lining and the balance of the flora. If these dominate your diet, the beneficial bacteria starve, while substances that burden the flora reach the gut in abundance.

You don't have to strive for perfection, and you don't have to change everything at once. The goal is to shift the balance: the more natural, minimally processed food on your plate — vegetables, fruit, legumes, whole grains, and, where your symptoms allow, gradually more fibre — and the less packaged, ultra-processed product. (Building the diet in detail is covered in a separate chapter; here the point is avoidance.) If your gut is sensitive, introduce fermenting, high-fibre foods step by step, watching your symptoms — in some cases a temporary, gentler (FODMAP^[G]-aware) approach can also help; discuss this with your treating physician.

Oral hygiene — the often-forgotten connection

Few of us would think that our mouth has anything to do with our gut flora — yet the oral cavity is the body's first microbiome station, and what happens there matters further down too. The bacteria living in the mouth continuously reach the gut by being swallowed; if the oral flora breaks down (e.g. untreated gum inflammation, periodontal disease), persistent, inflammation-promoting bacteria can pass from it into the gut, and this can burden the balance of the gut flora too. The good news is that this is exactly the kind of area you can keep in hand with simple daily habits.

The point is not complicated: regular, twice-daily toothbrushing, cleaning between the teeth (floss or interdental brush), and — something many people skip — gently cleaning the tongue, because plaque and bacteria settle on the back of the tongue too. It is also worth keeping up regular dental check-ups, because untreated gum and periodontal disease is a quietly persisting source of inflammation.

One caution: use strong, antiseptic (bacteria-killing) mouthwashes only in moderation, and not as a persistent daily routine, unless your dentist specifically recommends it. These too do not discriminate — they kill off the beneficial bacteria of the mouth as well — so their persistent, unjustified use can actually reduce the diversity of the oral flora. The daily basis is mechanical cleaning (brush, floss); mouthwash is at most a supplement.

Medication review — go through what you take, with your doctor

Beyond the PPI, it is worth going through your long-term medications with your doctor from time to time. Many people have for years been taking agents that were started for an old complaint, and since then no one has questioned whether they are still needed. The period after CDI is a good occasion for just such a "medication stocktake".

Pay particular attention to two groups. One is the acid suppressant (PPI), discussed above. The other is unnecessary or repeated antibiotics: if you frequently get antibiotics on a "just to be safe" basis, each time this thins out your protective gut flora again. Besides these, agents that slow gut motility or dry out the mouth and gut (some antispasmodics, anticholinergic medications) can also affect the flora and the symptoms.

The rule here is the same as with the PPI: never stop or change a medication on your own. Your task is to list what you take and ask the question, "is each one still justified?" — the weighing-up and the decision are your treating physician's. Often it is precisely such a review that reveals that something is no longer needed, or that there is a gentler alternative for the gut.

🍽️ Eating during these days

The theme of this week is what is worth avoiding, and one of its pillars is precisely eating: the concrete task of day 57 is to review how much ultra-processed food there is in your home and to start shifting the balance — swap at least one such product for a natural alternative (water instead of soft drink, fruit instead of crisps), and introduce fibre and fermenting foods gradually, watching your symptoms. The other two days (antibiotic awareness — day 55; reviewing the medication list — day 56) support eating indirectly: the fewer the substances burdening the flora, the better a nourishing diet is put to use.

For these days, the Plant Calendar (Appendix F) recommends steamed broccoli (day 55), steamed cauliflower (day 56) and kale (day 57) — three cruciferous vegetables, steamed, gently prepared. These days fall into the calendar's "diversity / fermentable fibres" (days 51–70) phase, where the aim is the active building of microbiome diversity. The fermentable fibre of cruciferous vegetables is the substrate of the fibre-degrading bacteria, from which short-chain fatty acids, including butyrate, are formed and nourish the gut lining — exactly the opposite of what a low-fibre, ultra-processed diet gives. These natural, minimally processed plants are thus practical examples of the balance-shift this chapter is about; with a sensitive gut, introduce them too gradually, steamed, watching your symptoms.

References

[159] Chassaing B, Koren O, Goodrich JK et al. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature. 2015. Link

In wild-type mice, relatively low concentrations of two ubiquitous emulsifiers — carboxymethylcellulose (CMC) and polysorbate-80 (P80) — induced low-grade inflammation and obesity/metabolic syndrome, and promoted robust colitis in mice predisposed to it. The mucus-protective barrier and microbiota composition were disrupted. The findings implicate dietary emulsifiers, ubiquitous components of processed foods, in the post-mid-20th-century rise in inflammatory bowel disease and metabolic disorders.

[160] Chassaing B, Van de Wiele T, De Bodt J, Marzorati M, Gewirtz AT. Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Gut. 2017. Link

Using the M-SHIME ex vivo human microbiota model that excludes host inflammation as a confounder, both carboxymethylcellulose (CMC) and polysorbate 80 (P80) acted directly on the human microbiota to increase its pro-inflammatory potential, evidenced by elevated bioactive flagellin. The CMC-induced flagellin rise was rapid (1 day) and driven by altered microbial gene expression. The findings establish that these dietary emulsifiers exert direct, host-independent pro-inflammatory effects on the human gut microbiota.

[218] Dethlefsen L, Relman DA. Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation. Proc Natl Acad Sci USA. 2011. Link

This longitudinal study examined the distal gut microbiota of three individuals over 10 months spanning two courses of ciprofloxacin, analyzing 1.7 million 16S rRNA sequences from 52-56 samples per subject. Interindividual variation dominated; baseline within-subject communities were stable over months. Ciprofloxacin profoundly reduced diversity and shifted composition within 3-4 days of initiation, with incomplete and individual-specific recovery. The findings characterize gut microbiota resilience and the durable disruption caused by repeated fluoroquinolone exposure.

[365] Reed AD, Theriot CM. Contribution of Inhibitory Metabolites and Competition for Nutrients to Colonization Resistance against Clostridioides difficile by Commensal Clostridium. Microorganisms. 2021. Link

This review examines how commensal Clostridium species mediate colonization resistance against C. difficile. Commensal Clostridia modify primary bile acids into secondary bile acids that suppress C. difficile spore germination and vegetative outgrowth. They additionally produce antimicrobial peptides and short-chain fatty acids that directly inhibit C. difficile and compete for limiting nutrients such as proline, important for C. difficile growth via Stickland fermentation. Loss of commensal Clostridia after broad-spectrum antibiotics is a key mechanistic step toward CDI susceptibility. The authors argue that restoring defined Clostridium consortia is a rational, mechanism-driven alternative to FMT for preventing recurrent CDI.