What bacteria really want

Last updated: Mar 31, 2026 | General

How does the microbiome work? What bacteria really want.

The attention that bacteria have received in recent years, driven by increasing microbiome research and a lifestyle industry based on it, has led to a shift in perception of what happens in our gut.
Suddenly, phrases like “the bacteria mean well for us” or “taking care of the microbiome” are gaining the upper hand and are more reminiscent of wellness than what it’s really about: microbiology.

How does the microbiome work? This question is often answered too simply. The humanization of the gut microbiome and its bacteria is a growing trend. There is nothing inherently wrong with making the complex processes in the gastrointestinal tract accessible and building wellness products on them. However, it is always important to classify it correctly: the human microbiome is a complex system consisting of thousands of different types of bacteria that work together symbiotically, coexist or fight each other.

None of what happens in our bodies down there serves the idea of wellness.

Although there are evolutionary constellations in which the microbiological metabolism is very closely linked to that of the host, this is not done on purpose, but because this particular state is particularly stable.

Basically, bacteria only pursue one goal that all living organisms have in common: Growth and reproduction.

Your gut is not a wellness temple

If we look at the colorful goings-on in our intestines from this rather sober perspective, it becomes clear that we do not run a wellness temple there, but follow a strict microbiological logic:

Your gut is not a beauty palace.

Your gut is a bioreactor.

But is this differentiation important? Yes, absolutely! Because if we stick to microbiological principles, we can influence our microbiome much more effectively and successfully. The benefits that arise from this knowledge are much more tangible than if the microorganisms are regarded as cute little buddies.

Controlling the bioreactor

The bioreactor in our body serves as a source of energy and is relevant for central physiological processes and mental stability.

Three factors influence every bioreactor and our gut microbiome in particular: substrate, space and time. If these are taken into account, the system can be positively influenced.

Factor 1: Substrate – lighting the fire

The substrate is the actual food for the bioreactor, for the fire that makes everything burn. In our large intestine, the majority of the 38 trillion bacteria in our microbiome are waiting to be fed. The system can actually shift very quickly in one direction. Studies suggest that the first adjustments to a change in substrate take place within a day. However, the system can return to its original state just as quickly if the corresponding substrate or substrate mixture is no longer supplied.

The aim of every intervention is to shift the bacteria in a direction that benefits health.

The formation of butyrate

An important process is the formation of butyrate, a short-chain fatty acid in the intestine with clearly described effects.
Important for its formation is the cross-feeding of bacteria, i.e. the metabolic association of several species, in which one bacterial species produces a substance that is further utilized by the next species. Here we must consistently think in terms of communities, never in terms of isolated bacteria. Many metabolic products, so-called metabolites, are therefore not end products but intermediate products in the complex microbial metabolic network.

Important producers include Faecalibacterium prausnitzii and Roseburia.

Butyrate is a central substance in the entire intestinal system.

It serves as a preferred energy source for the cells of the intestinal wall, the colonocytes. This increases oxygen consumption in the intestinal wall, which suppresses the growth of facultative anaerobic opportunists, i.e. bacteria that can also grow well in the presence of oxygen.
At the same time, it strengthens the intestinal barrier by promoting the expression of certain proteins and increasing mucin production by goblet cells. This leads to a lower permeability of the intestinal barrier – it becomes more permeable.
Furthermore, butyrate intervenes in immunological processes and modulates inflammatory reactions. Other effects such as influences on tumor biology, insulin sensitivity or the gut-brain axis have been described, but are context-dependent.

The key point is that it is not a question of more butyrate being better. The effect depends on the availability of the substrate, the structure of the microbial population and the localization in the intestine. It is therefore not enough to simply add butyrate. Butyrate must be in the right place at the right time.

Butyrate is a functional hub between microbial activity and human metabolism.

The high-protein diet

A diet high in protein and low in fiber has also been well studied and can shift populations to such an extent that harmful substances such as ammonia, p-cresol and secondary bile acids increase and butyrate production decreases. Studies therefore show that it is important to increase fiber intake accordingly when eating a high-protein diet.

Factor 2: Space – occupying the niche

The space available for the bacteria to attach to the intestinal wall is limited and usually already fully occupied. A new bacterium must therefore secure an advantage in order to gain one of the coveted places.

Colonization resistance

This is the principle of colonization resistance, in which the existing bacteria prevent new ones from attaching themselves to the intestinal wall. This often acts as protection against pathogenic germs that cannot find a place if the niches are already occupied. If a bacterium has no opportunity to colonize, it is flushed out via the rectum.

Studies have impressively shown that antibiotics radically eliminate the intestinal flora and thus abruptly reduce resistance to colonization. This allows opportunistic germs to occupy niches to which they previously had no access. Colonization of the intestinal wall should therefore not be thought of as a free apartment. There are no free apartments that can be entered at will. In principle, the situation is comparable to a packed soccer stadium.

Even if the new soccer fan is loaded down with a huge number of beer cans to give away, if there is no space available, he is simply pushed on.

Bacteriocins

The niches are not only occupied by the bacteria, but are also actively defended. For example, through bacteriocins, so-called bactericidal agents, which are released by the inhabitants to kill off new competitors. However, lowering the pH value is another tool used to secure the “home” or “stadium space”, as is the creation of oxygen gradients so that only certain bacteria can survive there. Niches directly in the mucin, an essential component of the mucus on our mucous membranes, can also provide additional retreats and give the inhabitants an advantage.

Antibiotics

This is also the particular danger of administering antibiotics. Killing the existing bacteria creates so-called ecological windows. Bacteria that previously had no chance, including opportunistic or pathogenic bacteria, can settle in the resulting free spaces and prevent the original inhabitants from returning. This can change the composition in the long term.

Factor 3: Time – slowly adapt to new things

Time is a key factor in the bioreactor. The example of fiber addition makes this clear: if the supply is suddenly increased significantly and the diet was previously low in fiber, the bacteria need time to adjust their metabolism. At the same time, specialized bacteria need time to multiply. Fibre that is not metabolized remains, attracts water and can lead to flatulence through opportunistic fermentation.

Time can be divided into several levels:

Transit time

Transit time is the time the bacteria need to pass through the intestine. The longer this is, the higher the probability that they will find a suitable docking site in the intestine. If the microorganisms do not manage to conquer a niche, they are flushed out with the stool. You can actually imagine this like passing through a sewer system. If they are unable to get out of the flow, the bacteria are mercilessly flushed out.

Sequence

The sequence of microbial processes is essential for the establishment of complex microbial networks. Most bacteria are interdependent and can only grow once others have done their preliminary work.

Time of day

The microbiome is subject to diurnal fluctuations, so the timing of substrate intake influences which bacteria benefit. This is particularly critical for people who have to work alternating day and night shifts. But “party animals” who like to go to bed later at the weekend also bring unrest to their microbiome.

How does the microbiome work? Substrate, space, time!

With knowledge of substrate, space and time, the understanding of the bioreactor becomes more precise. However, if you have a better understanding of the bioreactor, you can also control it better. You can visualize it as a boiler in which you have these three control variables at your disposal and can influence the output of the bioreactor through the associated changes.

A bioreactor system can be classified as stable and healthy if:

1. the substrates are converted efficiently and no harmful by-products are formed.
2. no single species dominates in such a way that others are displaced.
3. the system has sufficient time to develop.

This balance in our gut, in the bioreactor, does not arise because the bacteria are particularly good to us, but because millions of individual growth interests limit each other. This means that only certain constellations are permitted.

This is classic ecology and not a state of wellness.

7 practical tips

With the knowledge of substrate, space and time, a conscious effort can be made to improve the condition of the gut microbiome.

1. which substrate?

Consciously choose which substrates, i.e. nutrients, you add, as this will promote specific microorganisms.

2. targeted selection

Make this choice purposefully and consistently. Once you have decided on a particular path, take your time and don’t switch back and forth quickly.

3. no overloading

Avoid overloading, even with generally favorable substrates. It makes no sense to eat kilos of lentils. Pay attention to balance.

4. space and time

Bear in mind that the space in your gut is limited for the microorganisms and that changes take time. Don’t expect miracles.

5. combine

If necessary, combine microorganisms from probiotics or fermented products with the appropriate substrates to give them an advantage. Synbiotics take exactly this approach.

6. weeks instead of days

Plan adjustments over periods of weeks, not days. Be patient.

7. caution reset!

Bear in mind that systems without continuous input can return to their original state. As a rule, the system changes again when you stop your new eating habits. You also don’t train with dumbbells for two weeks and then expect increased muscle strength for the rest of your life.

Impulse: The adaptation cycle

Choose a single substrate, plant or fiber that you haven’t added to your diet before. This could be pulses or a particular root vegetable.

Start with a small dose, preferably just a teaspoon, not a bowl full. Then slowly increase the dose. Observe your body; give the system time. Don’t think in terms of hours or days, but weeks. Make a note of the changes, otherwise you will forget them again. When your system has adapted to the substrate, add another substrate and start the cycle again.

You are your own designer

Changing microbial systems is not a short-term process. If you think of the image of the bioreactor, you have to adjust the selection conditions in such a way that the growth of the bacteria is shifted in a direction that supports you.

Continuous observation and documentation is therefore advisable.

And so back to the initial question: How does the microbiome work?
Not about morality, not about “good” or “bad”.
But about substrate, space and time.

This turns a rather diffuse process into a controllable system.

Because at the end of the day, bacteria only want one thing: growth.
And it’s up to you to set the conditions for this.

Bibliography and further reading

Bry L, Falk PG, Midtvedt T, Gordon JI. A model of host-microbial interactions in an open mammalian ecosystem. Science. 1996. https://doi.org/10.1126/science.273.5280.1380

Byndloss MX, Olsan EE, Rivera-Chávez F, et al. Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. Science. 2017. https://doi.org/10.1126/science.aam9949

Dapa T, Serotte Ramiro R, Pedro MF, Gordo I, Xavier KB. Diet leaves a genetic signature in a keystone member of the gut microbiota. Cell Host Microbe. 2022. https://doi.org/10.1016/j.chom.2022.01.002

Derrien M, Vaughan EE, Plugge CM, de Vos WM. Akkermansia muciniphila gen. nov., sp. nov., a human intestinal mucin-degrading bacterium. Int J Syst Evol Microbiol. 2004. https://doi.org/10.1099/ijs.0.02873-0

Devkota S, Wang Y, Musch MW, et al. Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. Nature. 2012. https://doi.org/10.1038/nature11225

Hillman EBM, Baumgartner M, Carson D, et al. Changing Gastrointestinal Transit Time Alters Microbiome Composition and Bile Acid Metabolism: A Cross-Over Study in Healthy Volunteers. Neurogastroenterol Motil. 2025. https://doi.org/10.1111/nmo.70075

Jahng J, Jung IS, Choi EJ, Conklin JL, Park H. The effects of methane and hydrogen gases produced by enteric bacteria on ileal motility and colonic transit time. Neurogastroenterol Motil. 2012. https://doi.org/10.1111/j.1365-2982.2011.01819.x

Martens EC, Chiang HC, Gordon JI. Mucosal glycan foraging enhances fitness and transmission of a saccharolytic human gut bacterial symbiont. Cell Host Microbe. 2008. https://doi.org/10.1016/j.chom.2008.09.007

Martínez I, Maldonado-Gómez MX, Gomes-Neto JC, et al. Experimental evaluation of the importance of colonization history in early-life gut microbiota assembly. eLife. 2018. https://doi.org/10.7554/eLife.36521

Minnebo Y, Delbaere K, Goethals V, et al. Gut microbiota response to in vitro transit time variation is mediated by microbial growth rates, nutrient use efficiency and adaptation to in vivo transit time. Microbiome. 2023. https://doi.org/10.1186/s40168-023-01691-y

Rivera-Chávez F, Zhang LF, Faber F, et al. Depletion of Butyrate-Producing Clostridia from the Gut Microbiota Drives an Aerobic Luminal Expansion of Salmonella. Cell Host Microbe. 2016. https://doi.org/10.1016/j.chom.2016.03.004

Roager HM, Hansen LBS, Bahl MI, et al. Colonic transit time is related to bacterial metabolism and mucosal turnover in the gut. Nat Microbiol. 2016. https://doi.org/10.1038/nmicrobiol.2016.93

Thaiss CA, Levy M, Korem T, et al. Microbiota Diurnal Rhythmicity Programs Host Transcriptome Oscillations. Cell. 2016. https://doi.org/10.1016/j.cell.2016.11.003

Thaiss CA, Zeevi D, Levy M, et al. Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. Cell. 2014. https://doi.org/10.1016/j.cell.2014.09.048

Vandeputte D, Falony G, D’hoe K, Vieira-Silva S, Raes J. Stool consistency is strongly associated with gut microbiota richness and composition, enterotypes and bacterial growth rates. Gut. 2016. https://doi.org/10.1136/gutjnl-2015-309618

Winter SE, Winter MG, Xavier MN, et al. Host-derived nitrate boosts growth of E. coli in the inflamed gut. Science. 2013. https://doi.org/10.1126/science.1232467

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