You Have the Microbiome That You Deserve
From Seoul to Soul
A microbiologist in Cork built a weapon that kills one pathogen and spares a thousand neighbours. Then he told me the weapon is not the point.
In a glass vessel in Colin Hill’s lab at University College Cork, hundreds of bacterial strains coexist. Drawn from two healthy human guts, representing roughly a hundred species each, all strict anaerobes, all sequenced. All of these strains originated from the human gut and were placed together in a model community that, while far simpler than an actual intestine, preserves some of the ecological relationships these organisms had when they shared a living human gut.
Into this community, Colin’s team introduced Clostridioides difficile, the hospital-acquired pathogen responsible for tens of thousands of deaths each year. Then they added a bacteriocin. Bacteriocins are tiny antimicrobial peptides produced naturally by one bacterium to kill its closest competitors; they are, in effect, the weapons bacteria evolved to wage war on each other. This particular one, called thuricin CD, had shown high specificity against C. difficile.¹
Thuricin CD knocked C. difficile down roughly a thousandfold. The rest of the community looked virtually untouched.
When they ran the same experiment with conventional antibiotics, the damage was indiscriminate. The community’s dominant bacterial families were displaced by opportunistic ones. Overall diversity collapsed. With metronidazole, a common broad-spectrum treatment, the community was devastated.¹
The precision was extraordinary. And the analogy Colin reached for was not medical. It was ecological.
"If you remove a single species from a highly complex ecosystem like a tropical rainforest, the system may well persist. But if getting at that one species requires removing six others, you’re no longer tweaking an ecosystem, you’re destabilizing it."
Some bacteriocins are active in the nanomolar range, orders of magnitude more potent per molecule than conventional antibiotics.¹ Some are so specific they will kill C. difficile and a handful of its close relatives while leaving everything else intact.
But Colin was careful about the lesson. Removing the pathogen without removing the niche it occupied is a temporary fix. If the conditions that allowed C. difficile to flourish have not changed, it will return. The lasting solution is not a better weapon. It is a changed environment, which, as ever, comes back to food.
The Gym Your Immune System Lost
Colin’s bacteriocin work is about precision: one weapon, one target, minimal damage. But he also holds a theory about why the microbiome matters that operates at the opposite end of the spectrum, a theory about bluntness.
He described a pattern he had noticed across probiotic trials for conditions like bloating, discomfort, and irritable bowel syndrome. The finding that stopped him was not that some probiotics worked. It was that most of them worked, regardless of species, strain, or formulation. Some used Lactobacillus. Some used E. coli. Entirely different organisms, often similar outcomes. Meta-analyses confirm the general trend: probiotics as a class show benefit over placebo for IBS symptoms, though the certainty of evidence remains low and the question of strain specificity is far from settled.²
Colin draws a different conclusion from this pattern. “Could it be”, he asked, “that the immune system evolved over millennia in constant contact with enormous numbers of microorganisms and is now understimulated?”
That hygiene, food processing, and the sterile conditions of modern life have removed most of those microbial encounters, and the immune system, left without enough to do, begins reacting to things it should ignore?
Food components. The body’s own tissues. The chronic, low-grade inflammation that underlies so many modern diseases. The immunologist Graham Rook formalized a version of this idea as the “Old Friends” hypothesis: mammals co-evolved with specific microorganisms that train regulatory T cells, and their absence in modern life drives allergies, autoimmunity, and inflammatory disease.³
If that is true, then what all those different probiotics are providing is not a specific therapy. They are exercise. A workout for an immune system that evolved to lift rocks but now sits in an office chair.
Colin and his colleagues tested the idea indirectly. Working with Mary Ellen Sanders and colleagues in the US, they classified foods from the NHANES database into low, medium, and high microbial density and applied the system to more than 74,000 Americans,⁴ then linked that intake to health outcomes. Every additional 100 grams of microbe-containing food eaten daily was associated with a lower BMI, a smaller waist circumference, higher HDL cholesterol, and less C-reactive protein in the blood.⁵ The associations were modest, and the design was cross-sectional, which means it can show the pattern but not prove the direction. Korean researchers repeated the analysis on their own national data, the KNHANES database, and found similar patterns.⁶
The correlation does not prove causation. People who regularly eat yoghurt and kimchi and kefir probably exercise more, earn more, and attend to their health in other ways. But the direction is consistent. And the practical takeaway is strikingly simple. If you can get people to swap processed food for fermented food, it does not matter whether they are doing it because they believe in the microbiome or because they like the taste. The outcome is the same.
“Think of your microbiome as a pet. Most people who are sedentary will still walk their dog every day. They will spend any amount of money on veterinary care. Ask those same people to take a 30-minute walk for their own health and many will find a reason not to.”
If the microbiome becomes the reason to eat better, move more, and stress less, then the mechanism almost does not matter. People care for things outside themselves in ways they refuse to care for themselves.
What Diet Can and Cannot Do
A 2024 APC review published in Nature Reviews Microbiology, with Catherine Stanton as senior author, mapped the microbial consequences of major dietary patterns.⁷ Mediterranean and high-fibre diets support a diverse microbiota that produces health-promoting metabolites and supports the immune system. Western and ketogenic diets favour different bacterial communities, some of which are associated with chronic inflammation and conditions like colitis and Crohn’s disease.
None of that is in dispute. But Colin offered a nuanced perspective. “Hundreds of studies have now examined the impact of diet on the microbiome”, he said. “Diet undoubtedly changes it. But when you look at the actual figures, the proportion of microbiome variation explained by diet is surprisingly small”.
I asked him to quantify it.
Two landmark studies published simultaneously in Science in 2016, the Dutch LifeLines-DEEP cohort and the Belgian Flemish Gut Flora Project, each with over a thousand participants, combined genetics, disease, medication, diet, exercise, and dozens of other factors.⁸ ⁹
Together, all measured variables accounted for between 7 and 19 percent of total microbiome variation, with diet explaining a subset of that range.
The remaining 80-plus percent is driven by factors we do not yet understand, likely dominated by the gut environment itself: the mucus lining, the 37-degree temperature, the anaerobic conditions that select for a specific community regardless of what you ate for breakfast.
This does not mean diet is irrelevant. It means the graphs that show dots shifting between dietary groups can exaggerate the biological significance of those shifts. A statistically significant change may represent a biologically small one. Whether that small change is nonetheless important for specific health outcomes is exactly the question that remains open.
You Have the Microbiome You Deserve
Colin said it casually, almost as a throwaway. Then he paused to let it land.
“Every action you have taken in your life, every meal, every antibiotic, every night of sleep or sleeplessness, every period of stress or calm, has selected for the microbial community now living in your gut.”
If you want a different one, you have to change what you are doing. You cannot simply ask for a better microbiome. You have to earn it.
He called it a provocation. You could say the same about your knees or your skin. But it carries the core insight. Your microbiome is not a lottery you were handed at birth. It is a living record of how you have lived. And unlike your genome, which is fixed at conception, the microbiome responds to change. The microbiome responds quickly to dietary change but reshapes slowly; lasting structural remodelling requires sustained effort over weeks to months.¹⁰
The conversation left me thinking of the microbiome as something as individual as a fingerprint. No two people carry the same community, not even identical twins raised under the same roof, because the ecosystem inside you reflects your own history of meals, medications, stresses, and exposures. And like any complex ecosystem, it resists simple interventions. Pull one species out and others move in to fill the gap. Add one and the community either absorbs it or crowds it out, depending on conditions you do not fully control.
This is why single-target approaches so often disappoint, and why the researchers I spoke with in Cork kept circling back to the same word: change. Not a single change but a sustained pattern, held long enough for the system to reorganize.
Paul Ross had made a similar point that morning. The question is not whether you can change your microbiome. It is whether you will reshape it in directions that support health rather than undermine it.
What Monday Looks Like
The best way to improve your microbiome, Colin said, is the best way to improve any aspect of your life. Change. Sleep, food, movement, connection. No supplement replaces those fundamentals, no test substitutes for them, no fad outlasts them. The microbiome is a lever we did not know about, translating those basics into biological reality. But it was always part of the equation. We just were not measuring it.
He makes his own kombucha. He eats more fermented foods than he used to, not because he has proven they work in a clinical trial, but because he likes them and they are healthy foods regardless of the microbial hypothesis. He eats more dates and high-fibre foods when the choice is available. Small shifts, not a reinvention.
“Do not ask what a healthy microbiome looks like. Ask what you are willing to change.”
Soul Inquiry
Your microbiome has been listening to every choice you have made. If it could talk back, what would it ask you for?
This is the second of six posts from my visit to APC Microbiome Ireland in Cork. Next: fermented foods from Cork to Korea to Japan, and why what is in that bottle may not be what you think.
Many thanks to everyone at APC who so generously gave their time during my visit. The science is theirs, and I am grateful for the opportunity to share it.
References
¹. Rea, M. C., Dobson, A., O’Sullivan, O., et al. (2011). Effect of broad- and narrow-spectrum antimicrobials on Clostridium difficile and microbial diversity in a model of the distal colon. PNAS, 108(Suppl 1), 4639-4644. https://doi.org/10.1073/pnas.1001224107
². Goodoory, V. C., Khasawneh, M., Black, C. J., Quigley, E. M. M., Moayyedi, P., & Ford, A. C. (2023). Efficacy of probiotics in irritable bowel syndrome: Systematic review and meta-analysis. Gastroenterology, 165(5), 1206-1218. https://doi.org/10.1053/j.gastro.2023.07.018
³. Rook, G. A. W. (2023). The old friends hypothesis: Evolution, immunoregulation and essential microbial inputs. Frontiers in Allergy, 4, 1220481. https://doi.org/10.3389/falgy.2023.1220481
⁴. Marco, M. L., et al. (2022). A classification system for defining and estimating dietary intake of live microbes in US adults and children. Journal of Nutrition, 152(7), 1729-1736. https://doi.org/10.1093/jn/nxac074
⁵. Hill, C., Tancredi, D. J., Cifelli, C. J., et al. (2023). Positive health outcomes associated with live microbe intake from foods, including fermented foods, assessed using the NHANES database. Journal of Nutrition, 153(4), 1143-1149. https://doi.org/10.1016/j.tjnut.2023.02.019
⁶. Zhao, N., Zhan, Y., Choi, J., Lee, H. J., & Chung, M. (2026). Associations between live dietary microbe intake and cardiometabolic health in Korean adults. Journal of Nutrition, 156(5), 101459. https://doi.org/10.1016/j.tjnut.2026.101459
⁷. Ross, F. C., Patangia, D., Grimaud, G., et al. (2024). The interplay between diet and the gut microbiome: Implications for health and disease. Nature Reviews Microbiology, 22, 671-686. https://doi.org/10.1038/s41579-024-01068-4
⁸. Zhernakova, A., Kurilshikov, A., Bonder, M. J., et al. (2016). Population-based metagenomics analysis reveals markers for gut microbiome composition and diversity. Science, 352(6285), 565-569. https://doi.org/10.1126/science.aad3369
⁹. Falony, G., Joossens, M., Vieira-Silva, S., et al. (2016). Population-level analysis of gut microbiome variation. Science, 352(6285), 560-564. https://doi.org/10.1126/science.aad3503
¹⁰. David, L. A., Maurice, C. F., Carmody, R. N., et al. (2014). Diet rapidly and reproducibly alters the human gut microbiome. Nature, 505, 559-563. https://doi.org/10.1038/nature12820