The Shared Human Microbiome — We Are Literally Connected

The human microbiome refers to the complete collection of microorganisms — bacteria, archaea, viruses, fungi, and other microbial eukaryotes — that inhabit the human body, along with their collective genetic material. It is most densely populated in the gastrointestinal tract, particularly the colon, but is also present on the skin, in the oral cavity, the respiratory tract, the urogenital tract, and other body sites.

The figures involved are difficult to hold in the mind. A 2016 revision of earlier estimates by Sender et al. in Cell put the number of bacterial cells in the human body at approximately 3.8 × 10^13 — roughly 38 trillion — compared to approximately 3.0 × 10^13 human cells. This ratio, once dramatically overstated as "10 to 1," is now understood to be approximately 1:1, varying by individual, body weight, and composition. But the sheer number of organisms is not the most important fact. The most important fact is what they do.

The collective genome of the human microbiome — the microbiome — contains approximately 150 times more genes than the human genome itself. These genes encode functions that the human genome does not. The microbiome synthesizes vitamins that humans cannot produce: vitamin K, biotin, folate, and several B vitamins. It ferments dietary fiber into short-chain fatty acids (butyrate, propionate, acetate) that serve as the primary energy source for colonocytes — the cells lining the colon — and have systemic anti-inflammatory effects. It trains and calibrates the immune system, particularly in early life, helping to establish the distinction between self and non-self, and between commensal (friendly) and pathogenic microbes.

The microbiome is not uniform. Different body sites host distinct microbial communities adapted to those sites' specific conditions. The gut microbiome is dominated by bacteria from the phyla Firmicutes and Bacteroidetes, though the precise composition varies enormously between individuals and within individuals over time. The skin microbiome varies by body site — the oily regions near sebaceous glands support different communities than dry or moist regions. Oral and vaginal microbiomes have their own characteristic compositions, the latter being distinctive in being relatively low in diversity under healthy conditions, dominated by Lactobacillus species.

The relationship between the gut microbiome and the brain — the gut-brain axis — is one of the most consequential and rapidly developing areas of biomedical research. What was once a fringe hypothesis has accumulated, over the past twenty years, into a body of evidence that has substantially changed how researchers understand mental health, neurodevelopment, and behavior.

The gut and brain communicate through multiple pathways. The vagus nerve — cranial nerve X — carries signals bidirectionally between the gut and the brainstem, with approximately 90% of the fibers carrying information from gut to brain, not the other way around. The gut is also home to the enteric nervous system: a dense network of approximately 500 million neurons embedded in the gastrointestinal wall that operates with significant autonomy and is sometimes called "the second brain." The gut produces and responds to neurotransmitters including serotonin, dopamine, GABA, and acetylcholine.

The most striking statistic is this: approximately 90-95% of the body's serotonin is produced in the gut, not the brain. Enterochromaffin cells in the gut lining synthesize serotonin, and gut bacteria play a critical role in regulating this production. The spore-forming bacteria of the gut have been specifically identified as influencing serotonin synthesis in enterochromaffin cells. Gut-derived serotonin does not cross the blood-brain barrier and does not directly regulate mood — that is important to clarify — but it plays critical roles in gut motility, nausea, and cardiovascular function. The relationship between gut serotonin dynamics and central serotonin function is bidirectional and complex, still being actively characterized.

What is clearer is the microbiome's influence on brain function through other routes. Gut bacteria metabolize tryptophan — the dietary amino acid that is the precursor to serotonin — through multiple competing pathways. The kynurenine pathway, activated by inflammation, produces neuroactive compounds including quinolinic acid (excitotoxic) and kynurenic acid (neuroprotective), and the balance between them is influenced by the microbiome. Short-chain fatty acids produced by microbiome fermentation cross the blood-brain barrier and influence glial cell function, neuroinflammation, and the integrity of the blood-brain barrier itself.

Animal studies have been striking. Germ-free mice — raised without any microbiome — display abnormal stress responses (exaggerated HPA axis reactivity), abnormal anxiety-like behavior, and altered social behavior. Transplanting microbiomes from humans with depression into germ-free rats has produced depression-like behaviors in those animals. Specific bacterial strains, particularly certain Lactobacillus and Bifidobacterium species, have demonstrated anxiolytic and antidepressant effects in animal models that operate through the vagus nerve — effects abolished when the vagus nerve is severed.

Human clinical trials are fewer and more complex to interpret, but the accumulating picture is consistent with a meaningful relationship between microbiome composition and mental health outcomes. Studies have found differences in microbiome composition in people with major depressive disorder, anxiety disorders, bipolar disorder, and autism spectrum conditions. The directionality — whether the microbiome changes cause or result from these conditions — is difficult to establish in humans, but the bidirectionality of the gut-brain axis suggests both directions operate.

The transmission of microbiome communities between people is not incidental. It is continuous and operates through multiple overlapping channels.

Vertical transmission. The first major microbiome colonization event in a human life is birth. During vaginal delivery, the infant is colonized by the mother's vaginal microbiome — predominantly Lactobacillus — as it passes through the birth canal. Infants born via caesarean section are instead colonized first by skin microbiota and environmental organisms, producing an initial microbiome composition that differs significantly from vaginally born infants. This difference has been linked to altered immune development and increased risk of conditions including asthma, allergies, and obesity, though the picture remains complex. Breastfeeding continues microbiome transfer: breast milk contains not just oligosaccharides that selectively feed specific beneficial bacteria, but living bacteria — including Bifidobacterium species that become dominant in the infant gut microbiome during breastfeeding.

Cohabitation effects. Spouses and long-term cohabitants share microbial communities to a degree not explained by similar diets or environments alone. A 2022 study in Nature examining over 9,000 people from three continents found that cohabiting partners were more similar in their gut microbiomes than would be expected by chance, and that this similarity increased with years spent together. The transmission operates through physical contact, shared surfaces, shared food, shared environment — and through behaviors that are themselves socially shaped. The researchers estimated that approximately 8-9% of the gut microbiome's variation could be explained by whether two people lived together.

Environmental and aerosol transmission. Humans continuously shed skin cells, hair, and microorganisms into the surrounding environment. Indoor spaces accumulate microbiome signatures from their occupants — buildings have been shown to carry microbial communities that reflect the people who live and work in them. Airborne transmission of microorganisms occurs in indoor spaces through respiratory aerosols. The microbiome of the air you breathe in a room is partly composed of microorganisms that were, minutes ago, on someone else's skin or in someone else's respiratory tract.

Pet and animal transmission. Households with dogs have different microbiomes than households without dogs, and this difference is shared among family members. Dogs bring environmental microbiota from outdoor environments, and close contact with pets produces ongoing bidirectional microbial exchange.

Community-level effects. Some research suggests detectable microbial community similarities at the level of geographic communities — shared water sources, shared food systems, shared built environments all producing convergences in microbiome composition that operate at scales larger than the household.

The microbiome is sensitive to a large number of factors, many of which are distributed unequally across society. Understanding these factors is important for understanding how microbiome health intersects with social determinants of health — and why individual microbiome health cannot be fully separated from collective conditions.

Antibiotics. A single course of broad-spectrum antibiotics can dramatically alter the microbiome, reducing diversity and eliminating sensitive species. Recovery can take weeks to months and may be incomplete — some species may not fully recover. Repeated antibiotic exposure, which is more common in settings with high rates of infectious disease or poor medical care, produces cumulative disruption.

Diet. The single strongest modifiable factor in adult microbiome composition is diet. High dietary fiber — from diverse plant foods — feeds a diverse microbiome and supports the production of short-chain fatty acids. Low-fiber, high-processed-food diets support different, less diverse microbial communities associated with increased inflammation. Access to dietary diversity is not equally distributed. Food deserts, food costs, and the economics of ultra-processed food production create conditions where populations with lower socioeconomic status are systematically more likely to have microbiome compositions associated with worse health outcomes.

Early life conditions. The first three years of life are a critical window for microbiome establishment. Conditions in this period — mode of birth, breastfeeding, antibiotic exposure, dietary diversity, environmental exposures, stress in the household — have long-lasting effects on microbiome composition and on the immune system calibration that the microbiome shapes. Early adversity — poverty, food insecurity, toxic stress — produces microbiome disruptions that persist into adult life and that are associated with elevated inflammatory markers, altered stress responses, and increased disease risk.

Chronic stress. The stress response directly alters the gut microbiome. Corticosteroids and catecholamines (stress hormones) affect gut motility, mucus production, and the local immune environment — all of which affect which organisms can thrive. Chronic stress reduces microbial diversity. Animal studies have demonstrated that social disruption stress alters the gut microbiome within days. This creates a feedback loop: stress disrupts the microbiome, microbiome disruption alters the gut-brain axis, and gut-brain axis alterations influence stress response, anxiety, and depression.

Environmental exposures. Pesticides, industrial chemicals, heavy metals, and other environmental contaminants affect the microbiome. These exposures are not equally distributed — they are concentrated in lower-income communities and communities of color through the mechanisms of environmental injustice.

The immune system is, in part, educated by the microbiome. The development of appropriate immune responses — calibrated to distinguish self from non-self, commensal from pathogen, and harmful from harmless — occurs in early life in dialogue with the colonizing microbial community.

The hygiene hypothesis (more precisely, the "old friends" hypothesis, as articulated by Graham Rook) proposes that the dramatic increases in autoimmune and allergic conditions in industrialized countries over the twentieth century are partly explained by reduced exposure to the microbial communities that co-evolved with the human immune system. The immune system, calibrated by evolutionary history to expect certain microbial inputs, behaves differently — more dysregulated, more prone to misdirected inflammatory responses — in their absence.

The microbiome is now implicated in conditions that extend well beyond the gut: multiple sclerosis, rheumatoid arthritis, type 1 and type 2 diabetes, cardiovascular disease, certain cancers, and neurodegenerative conditions including Parkinson's disease. The relationship is bidirectional in most cases — disease states alter the microbiome, and microbiome alterations contribute to disease progression — but the centrality of the microbiome to systemic health has become impossible to ignore.

Parkinson's disease deserves specific mention. Research by Marios Hadjigeorgiou, Heiko Braak, and others has suggested that Parkinson's may, in many cases, begin in the gut — with the misfolding of alpha-synuclein protein occurring first in enteric neurons and spreading via the vagus nerve to the brainstem and eventually the substantia nigra. The microbiome of Parkinson's patients differs from that of matched controls. This doesn't make Parkinson's a microbiome disease in a simple sense, but it places the gut — and by extension the microbial community that shapes gut function — at the origin of what we previously thought was purely a brain disease.

The microbiome does something unusual to the concept of the individual.

We have inherited, from a long Western philosophical tradition, the idea of the individual as a discrete, bounded unit — a body with a clear inside and outside, a self with a clear definition of what belongs to it and what doesn't. The microbiome doesn't fit this model. The organisms that live inside your gut are not you — they have their own genomes, their own evolutionary histories, their own interests. But they are also not not-you. Remove them, and your health fails. They are constitutive of your normal functioning. They are symbiotes so integrated that the line between host and microorganism has become genuinely difficult to draw.

Philosopher of biology Myra Hird and others have written about the way microbiology challenges the model of the bounded individual. The microbiome is just one instance of a larger pattern: the human body is not a closed system. It is an open system continuously exchanging matter and organisms with its environment and with other human bodies.

This matters for how we think about health policy, about responsibility, about connection. If my wellbeing is partly constituted by microbial communities that I share with the people around me, then my health cannot be fully separated from theirs. The conditions that shape their microbiomes — poverty, stress, environmental contamination, food access — ripple into mine, and mine into theirs. Not metaphorically. Literally, through shared organisms.

The most dramatic demonstration of the microbiome's power — and of its shareability — is fecal microbiota transplantation (FMT).

FMT involves transferring a processed sample of stool from a healthy donor into the gastrointestinal tract of a recipient. The result is a rapid reconstitution of the recipient's microbiome with the donor's community. The primary clinical application, and the one with the most robust evidence, is treatment of recurrent Clostridioides difficile (C. diff) infection — a devastating gut infection that is very difficult to treat with antibiotics and that kills thousands of people annually. FMT has shown cure rates above 90% in clinical trials for recurrent C. diff — far higher than any antibiotic regimen.

The implications extend further. FMT is being studied for inflammatory bowel disease, metabolic syndrome, autism spectrum conditions, Parkinson's disease, and several mental health conditions, with varying degrees of evidence and clinical promise. The ongoing work represents a fundamental recognition that the microbiome community as a whole is a transferable, functional unit — and that a sick microbiome can, literally, be replaced with a healthier one from another person.

You can save someone's life by giving them someone else's gut bacteria. That's a sentence that makes the abstract concrete. The microbiome is shared, is sharable, and the sharing can be the cure.

Eat for diversity. The single most impactful thing you can do for your microbiome is increase the diversity of plant foods in your diet. The American Gut Project found that people who ate 30 or more different plant types per week had significantly more diverse microbiomes than those who ate fewer. You're not eating for macronutrients. You're farming.

Notice the social microbiome. Pay attention to physical contact, shared meals, and time in shared spaces as microbial exchange events — not to be squeamish about them, but to recognize that they are actual exchanges of biological material. The warmth you feel in close connection with people you trust has a physical substrate. Some of it is microbial.

Protect your gut during stress. Chronic stress is a microbiome disruptor. The stress-gut connection runs both ways. Managing stress isn't just about your mind — it's about maintaining the ecosystem inside you that your mental health depends on. Sleep, fiber-rich food, social connection, and time in natural environments are all evidence-backed microbiome protectors.

Take antibiotics when necessary, not casually. A course of antibiotics is a significant event for the ecosystem inside you. It's often the right call. But it should be a considered one, not a reflexive one. Probiotic support and fiber during and after a course can support recovery, though the evidence for specific protocols is still developing.

Spend time in natural environments. Emerging research on the "biodiversity hypothesis" suggests that exposure to diverse natural environments — soil, plants, outdoor air — increases the diversity of your microbiome through environmental exposure. Urban environments, particularly those lacking green space, produce less diverse microbial exposures. The design of cities has microbiome consequences.

---

1. Sender, R., Fuchs, S., & Milo, R. (2016). Revised estimates for the number of human and bacteria cells in the body. Cell, 164(3), 337–340.

2. Turnbaugh, P. J., Ley, R. E., Hamady, M., Fraser-Liggett, C. M., Knight, R., & Gordon, J. I. (2007). The human microbiome project. Nature, 449(7164), 804–810.

3. Cryan, J. F., O'Riordan, K. J., Cowan, C. S. M., et al. (2019). The microbiota-gut-brain axis. Physiological Reviews, 99(4), 1877–2013.

4. Yano, J. M., Yu, K., Donaldson, G. P., et al. (2015). Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell, 161(2), 264–276.

5. Valles-Colomer, M., Falony, G., Darzi, Y., et al. (2019). The neuroactive potential of the human gut microbiota in quality of life and depression. Nature Microbiology, 4(4), 623–632.

6. Moeller, A. H., Suzuki, T. A., Phifer-Rixey, M., & Nachman, M. W. (2018). Transmission modes of the mammalian gut microbiota. Science, 362(6413), 453–457.

7. Valles-Colomer, M., Bacigalupe, R., Vieira-Silva, S., et al. (2022). Variation and transmission of the human gut microbiota across multiple familial generations. Nature Microbiology, 7(4), 476–489.

8. Rook, G. A. W. (2013). Regulation of the immune system by biodiversity from the natural environment: An ecosystem service essential to health. Proceedings of the National Academy of Sciences, 110(46), 18360–18367.

9. Kelly, C. R., Kahn, S., Kashyap, P., et al. (2015). Update on fecal microbiota transplantation 2015: Indications, methodologies, mechanisms, and outlook. Gastroenterology, 149(1), 223–237.

10. Dinan, T. G., Stanton, C., & Cryan, J. F. (2013). Psychobiotics: A novel class of psychotropic. Biological Psychiatry, 74(10), 720–726.

11. McDonald, D., Hyde, E., Debelius, J. W., et al. (2018). American gut: An open platform for citizen science microbiome research. mSystems, 3(3), e00031-18.

12. Braak, H., de Vos, R. A. I., Bohl, J., & Del Tredici, K. (2006). Gastric alpha-synuclein immunoreactive inclusions in Meissner's and Auerbach's plexuses in cases staged for Parkinson's disease-related brain pathology. Neuroscience Letters, 396(1), 67–72.

13. Hird, M. J. (2009). The Origins of Sociable Life: Evolution After Science Studies. Palgrave Macmillan.

14. Sonnenburg, J., & Sonnenburg, E. (2015). The Good Gut: Taking Control of Your Weight, Your Mood, and Your Long-Term Health. Penguin Press.