III. 1 Supporting engraftment

The FMT set recovery in motion, but the flora you have taken in must also find a home in you. In the next three days you learn what engraftment is, and how to help it with small daily decisions, so that the new bacteria truly stay.

What does engraftment mean?

Imagine that the implanted flora is like a freshly sown garden that we keep seeding. The seeds have been scattered – that was the FMT course – but for them to sprout and take root, they need the right soil, water and light. The same happens in the gut: the beneficial bacteria^[G] you have taken in need nourishment and a calm environment in order to multiply and engraft durably. This process is what we call engraftment^[G].

The difference between a medicine and a living preparation becomes tangible precisely here. A painkiller works even if you eat pizza and sleep little afterwards. The living gut flora, by contrast, responds to how you live – a change of diet shifts its composition within 24 hours (David 2014 [110]): if you feed it and do not disturb it, it grows stronger; if you starve it or churn it up again, it has a harder time staying. The good news is that you can influence this yourself, and with simple, everyday tools at that.

Engraftment is not the work of a single day, but a process of weeks and months. In the coming weeks we will gradually build up the habits – fibre, plant variety, fermented foods, rest – that keep this garden alive. We do not want to keep sowing forever; we want to tend the life now being planted. For now we begin with the basics: with conscious hydration, with the first fibres, and with not disturbing the freshly arrived flora.

The protected window: now is the time to change

The “protected window” is an image, not a physiological state – but the idea behind it is simple. As long as you take the daily capsule, the incoming flora is replenished day after day: a bad day, a missed portion of fibre or a poor night’s sleep will not upset the balance, because the capsule is holding it. So you do not have to get everything a hundred per cent right – and that is exactly what makes this period suitable for calmly practising the new habits.

After the capsules, however, the support ends, and from then on what counts is what you built in the meantime. So do not wait until the end of the course: let the daily fibre, the variety of plants and the calm evening settle in now, under protection – so that when the capsules run out, the habits hold the balance. Engraftment is not random either: the donor strains that persist are those that have somewhere to move into within your own community (Smillie 2018 [108]) – and your diet is what shapes that environment.

What helps and what hinders engraftment?

The most important helper is nourishment. The beneficial bacteria live primarily on fibres^[G], which we ourselves cannot digest – but they can. This is why, already in these days, we begin to bring small fibre sources into the meals: a handful of oats, a few bites of vegetables, an apple. You do not need to switch to a drastic diet, only to pair something plant-based with every meal.

The most important hindering factor is the very thing that set all of this in motion: antibiotics. This is why, during and after the course, you must avoid any antibiotic that you do not absolutely need – and if for any reason you are still given one, always tell the treating physician managing your FMT as well. Similarly to be avoided during the course are the shop-bought probiotic preparations, because they can churn up the freshly forming balance. Calm matters too: lasting stress and lack of sleep affect the composition of the gut flora and the intestinal barrier as well (Karl 2018 [109]; Bishehsari 2025 [105]), which is why in these days we pay as much attention to rest as to diet.

🍽️ Eating during these days

In these three days the theme is supporting engraftment – and one of the most important tools for this is eating itself. Your tasks: take the daily dose according to the usual routine, drink plenty of fluid, do not start an antibiotic or probiotic course on your own, and pair something gentle and plant-based with every meal – on day 25 a first fibre source, on day 26 avoid the abundant sugary, processed food, and on day 27 already bring a small fibre to each of two different meals. Always drink enough water with the fibre, to make digestion easier; if the bloating intensifies, ease off the amount a little – this is not a race.

For these days, the Plant Calendar, in the firming foundation phase, recommends sources providing soluble fibre and resistant starch: on day 25 cooked sweet potato (soluble fibre, gentle), on day 26 gum arabic (acacia fibre) (gentle soluble fibre), and on day 27 resistant starch^[G] – cooled, cooked rice or potato – which is an excellent source of butyrate. These fibres feed the now-engrafting flora in the colon and support a firmer stool while the symptoms settle. Build the plant of the day into at least one meal, prepared gently; if you do not tolerate one of them well, reduce its portion and return to it later.

Why does this matter?

The FMT only sets recovery in motion – the durable result is decided by whether the new flora can engraft in you. In these days you have learned that you can help this yourself: you feed the beneficial bacteria with a little fibre, and you do not disturb them with unnecessary antibiotics or probiotics. In the coming weeks we will build further on exactly this foundation, step by step.

References

[003] 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 conclude from this that new therapies against CDI are urgently needed; the clinical validation of defined *Clostridium* consortia comes not from this review but from the VE303 phase 2 trial [56].

[010] Gregory AL, Pensinger DA, Hryckowian AJ. A short chain fatty acid-centric view of Clostridioides difficile pathogenesis. PLoS Pathog. 2021. Link

This review synthesizes the role of short-chain fatty acids (SCFAs) in C. difficile colonization resistance. The gut microbiome produces acetate, propionate and butyrate via fiber fermentation; these SCFAs maintain epithelial barrier function, modulate immunity and signal directly to C. difficile. The authors propose a conceptual model in which C. difficile senses the SCFAs themselves as a marker of a healthy, competitive gut environment and, in response, increases toxin production in order to sustain the dysbiotic state that favours it. SCFAs influence toxin production and competition with commensals. The review argues that targeting SCFA pathways — through dietary intervention, next-generation probiotics or other targeted approaches — offers a precision, non-antibiotic strategy against CDI distinct from both antibiotics and faecal transplant.

[014] Whelan K, Bancil AS, Lindsay JO, Chassaing B. Ultra-processed foods and food additives in gut health and disease. Nature Reviews Gastroenterology & Hepatology. 2024. Link

Critical review of how ultra-processed foods (UPFs) and the additives they contain affect gut health. The link between UPF-rich diets and gut disease — inflammatory bowel disease, colorectal cancer, irritable bowel syndrome — rests mainly on observational epidemiology, whereas the effects of individual additives (emulsifiers, sweeteners, colours, micro- and nanoparticles) come largely from in vitro and animal work showing impacts on the gut microbiome, intestinal permeability and inflammation. The authors stress that human intervention studies remain scarce, so the direction of the association is well supported while the size of the effect is still uncertain.

[033] Dethlefsen L, Relman DA. Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation. Proceedings of the National Academy of Sciences of the United States of America. 2011. Link

Stanford-based longitudinal study tracking the gut microbiota of three individuals over 10 months across two consecutive courses of ciprofloxacin, with deep 16S rRNA sequencing. Loss of bacterial diversity was profound and rapid, occurring within 3-4 days of antibiotic initiation, and recovery toward the pre-treatment state was often incomplete months after cessation. Repeated antibiotic exposure produced incremental, non-recoverable shifts in community composition. With over 2,000 citations, this paper is the canonical reference establishing that antibiotic-induced dysbiosis is not a self-correcting disturbance but can leave a lasting ecological imprint – central to the case for MTT in patients with cumulative antibiotic exposure history.

[048] Weingarden A, González A, Vázquez-Baeza Y, Weiss S, Humphry G, Berg-Lyons D, Knights D, Unno T, Bobr A, Kang J, Khoruts A, Knight R, Sadowsky MJ. Dynamic changes in short- and long-term bacterial composition following fecal microbiota transplantation for recurrent Clostridium. difficile infection. Microbiome. 2015. Link

Longitudinal microbiome characterisation following FMT in four patients with recurrent CDI, sampling daily for 28 days and weekly to 84 days post-treatment, over a total of 151 days. The recipient microbiota rapidly normalised from a markedly dysbiotic state to a healthy-range composition within days. Composition continued to change thereafter, diverging from the original donor implant material and fluctuating dynamically over both the short and the long term – while remaining throughout within the cloud of healthy microbiota. The paper supports the framing in this Guide that successful MTT produces a self-sustaining recipient ecology, not a permanent donor-tracked imprint.

[089] Bonomini-Gnutzmann R, Plaza-Díaz J, Jorquera-Aguilera C, Rodríguez-Rodríguez A, Rodríguez-Rodríguez F. Effect of Intensity and Duration of Exercise on Gut Microbiota in Humans: A Systematic Review. International journal of environmental research and public health. 2022. Link

Exercise intensity and duration determine gut microbiota composition; moderate exercise is favorable, while extreme endurance load may cause negative microbiota changes — 13 studies: intense exercise — increased gut permeability, elevated I-FABP, dysbiosis; 7 studies: moderate exercise — increase in microbial diversity and SCFA metabolites; in athletes, more adverse effects at high intensity (IJERPH, 2022).

[098] Karmisholt Grosen A et al. Effects of clinical donor characteristics on the success of faecal microbiota transplantation for patients in Denmark with Clostridioides difficile infection: a single-centre, prospective cohort study. The Lancet Microbe. 2025. Link

Single-centre, prospective Danish cohort: clinical donor characteristics — including antibiotic exposure in the 12 months before donation and donation stool consistency — affect FMT success in recurrent C. difficile infection; donor antibiotic use worsens outcomes, supporting strict donor screening.

[105] Bishehsari F, Post Z, Swanson GR, Keshavarzian A. Circadian Rhythms in Gastroenterology: The Biological Clock's Impact on Gut Health. Gastroenterology. 2025. Link

Review of the role of circadian rhythm in normal gastrointestinal function. The central clock in the hypothalamus and the peripheral clocks in GI organs together orchestrate gut function in response to environmental cycles; this clock is set by cues including light, **sleep** and eating times. Disruption of the rhythm — night-time light exposure, travel across time zones, shift work, mistimed eating, social jet lag — affects GI processes directly: digestion, absorption, **motility**, intestinal barrier function, immune function and the **microbiome**. The paper also discusses circadian-based interventions. Important for the handbook: the article links rhythm disruption to motility and the microbiome — it does NOT claim that sleep deprivation as such accelerates intestinal transit.

[108] Smillie CS, Sauk J, Gevers D, Friedman J, Sung J, Youngster I, Hohmann EL, Staley C, Khoruts A, Sadowsky MJ, Allegretti JR, Smith MB, Xavier RJ, Alm EJ. Strain Tracking Reveals the Determinants of Bacterial Engraftment in the Human Gut Following Fecal Microbiota Transplantation. Cell Host Microbe. 2018. Link

Strain-level tracking after FMT: the authors examined what determines whether a given donor strain engrafts in the recipient. The strongest predictor is the **composition of the recipient's own community** — a strain engrafts when a relative is already present, or when a free ecological niche exists; donor strain richness and strain abundance also matter. Engraftment therefore follows ecological rules rather than chance, and is modifiable from the recipient's side. Important: the paper describes strain-level determinants; it does not prove fibre availability as a modifiable factor in an RCT.

[109] Karl JP, Hatch AM, Arcidiacono SM, Pearce SC, Pantoja-Feliciano IG, Doherty LA, Soares JW. Effects of Psychological, Environmental and Physical Stressors on the Gut Microbiota. Front Microbiol. 2018. Link

Review of how psychological, environmental and physical stressors affect the gut microbiota. The authors argue that various stressors — including sleep deprivation, thermal load, altitude and psychological stress — alter microbiota composition and function through the gut-brain axis and impair intestinal barrier integrity. Important for the handbook: this is a **review**, largely based on animal work and controlled human stress models; it does NOT claim that stress or sleep loss impairs FMT engraftment.

[110] David LA, Maurice CF, Carmody RN, Gootenberg DB, Button JE, Wolfe BE, Ling AV, Devlin AS, Varma Y, Fischbach MA, Biddinger SB, Dutton RJ, Turnbaugh PJ. Diet rapidly and reproducibly alters the human gut microbiome. Nature. 2014. Link

Controlled human intervention study: volunteers consumed an exclusively animal-based, then an exclusively plant-based diet for a short period. Gut microbiota composition and gene expression changed **within 24 hours** and largely reverted after the diet ended. The animal-based diet increased bile-tolerant organisms and decreased strains that ferment plant polysaccharides. This is the classic evidence that the gut flora is a **living system that responds to how we live**, not a static state. Important: short-term, small-sample study, not in an FMT population and not about engraftment.