Clean Freak or Booger Eater?

Finding the Right Balance of Hormetic Stressors

The epidemiology of the last century tells a strange story: As industrialised nations got cleaner, with municipal water treatment, sewage systems, indoor plumbing, and broad-spectrum antibiotics, two things happened simultaneously. Infectious disease mortality dropped, and rates of allergic and autoimmune disease climbed. Asthma, eczema, hay fever, type 1 diabetes, inflammatory bowel disease, multiple sclerosis, and food allergies all rose across the twentieth century in ways that geographic and historical comparisons suggest are not simply diagnostic artefacts. Something about the modern environment was producing immune systems that attacked the wrong targets.

The dominant explanation, developed across decades from David Strachan’s original 1989 observation to the current biodiversity hypothesis, is that the human immune system requires specific environmental exposures during development to train itself properly. Removing those exposures (through over-sanitisation, antibiotic overuse, the rise of C-section delivery, the decline of breastfeeding, the move from farms to cities, the loss of soil and animal contact, the homogenisation of the modern diet) produces immune systems that are simultaneously more reactive to things that should not provoke them (allergens, the body’s own tissues) and less able to handle things they should (gut microbes, environmental pathogens at low levels).

I. The Hygiene Hypothesis Origin Story

David Strachan, a British epidemiologist, published a short paper in the British Medical Journal in 1989 titled “Hay fever, hygiene, and household size.” Working with data from 17,414 British children, Strachan found that hay fever and eczema were less common in children from larger families, particularly those with older siblings. His proposed explanation: older siblings expose younger ones to childhood infections, and this exposure during a critical developmental window trains the immune system away from allergic responses.

The 1989 paper named the hypothesis “hygiene hypothesis” because the framework implicated improved hygiene (smaller families, less child-to-child infection transmission, cleaner homes) as the proximate cause of rising allergic disease. The name has caused decades of confusion because the relevant exposures, as subsequent research clarified, aren’t really about hygiene as that word is commonly understood. The original framing implied that ordinary infections protect against allergy. Subsequent work showed the picture is different.

What survived from Strachan’s original observation: the empirical finding that children with more siblings, who attend daycare early, who live on farms, or who otherwise have rich early microbial environments show lower rates of allergic disease. The robustness of this finding across populations, decades, and study designs is strong.

II. Old Friends, Not Lost Infections

Graham Rook, professor of medical microbiology at University College London, proposed a refinement in 2003 that has become the dominant framework. Rook’s “old friends” hypothesis argues that the relevant exposures aren’t childhood infections per se but a class of organisms that co-evolved with humans across deep evolutionary time.

These “old friends” include:

• Helminths (parasitic worms that infected most humans across most of history)
• Environmental mycobacteria (non-pathogenic soil and water bacteria related to but distinct from the pathogenic ones)
• Saprophytic bacteria from soil and decomposing organic matter
• Commensal bacteria, fungi, and archaea that constitute the human microbiome
• Certain viruses that establish chronic asymptomatic infection (like CMV)

Rook’s argument: these organisms aren’t really infections in the disease-causing sense. They’re long-term residents and visitors that the human immune system evolved alongside, and that the immune system relies on for proper development. Their loss in modernised environments produces immune systems that lack the regulatory training these organisms provide.

The mechanism that makes this picture biologically coherent is regulatory T cell (Treg) education. Treg cells are the immune system’s brake pedal, the cells that prevent inflammatory responses from running unchecked. Exposure to old friends during early development drives the differentiation and proper function of regulatory T cells. Without that education, the immune system has the accelerator (effector T cells) without the brake (Tregs), producing the inflammatory diseases of modernity.

If childhood infections protect against allergy, the practical advice is to expose children to infections, which is dangerous and ethically problematic. If ancient commensal exposures protect against allergy, the practical advice is to allow children appropriate contact with soil, animals, dirt, and other sources of old-friend organisms while still maintaining hygiene against actual pathogens.

III. The Microbiome Picture

The decade after Rook’s 2003 paper saw a transformation of microbiology driven by high-throughput sequencing. The Human Microbiome Project, launched in 2007 by the US National Institutes of Health, produced the first systematic mapping of the microbial communities that inhabit and constitute most of the cells in the human body. What emerged was a picture of humans as super-organisms: roughly equal numbers of human cells and microbial cells, with microbial genes outnumbering human genes by perhaps 100 to 1.

The microbiome research transformed the hygiene hypothesis from a story about specific environmental exposures into a broader picture of microbial communities and their effects on host physiology. Key contributors:

• Martin Blaser, then at NYU, articulated in Missing Microbes (2014) the case that broad-spectrum antibiotic use, particularly in early childhood, has depleted the microbial diversity of populations in industrialised nations across generations. Blaser’s research focused initially on Helicobacter pylori, the bacterium associated with peptic ulcers, which has been largely eliminated from populations in industrialised countries through antibiotic eradication. While this has reduced ulcer disease, Blaser’s work suggests H. pylori loss may have contributed to rising rates of asthma, allergic diseases, and oesophageal disorders, because the bacterium also performs regulatory functions that haven’t been adequately appreciated.
• Justin and Erica Sonnenburg at Stanford have produced foundational work on the dietary determinants of microbiome diversity. Their book The Good Gut (2015) synthesises their research showing that low-fibre Western diets produce reduced microbial diversity within a generation, and that this reduced diversity is heritable across generations in mouse models. Their broader argument: even if you grew up with rich microbial exposures, eating a modern industrialised diet starves the diverse microbial community your body would otherwise sustain.
• Rob Knight at UCSD founded the American Gut Project, which has sequenced microbiomes from tens of thousands of participants. His work with Jack Gilbert, synthesised in their popular book Dirt Is Good (2017), brings the microbiome research into accessible, practical advice for parents. Their core position: most childhood concerns about exposing children to dirt, animals, and environmental microbes are misplaced.
• Susan Lynch at UCSF has produced significant work on infant microbiome development and its relationship to subsequent allergic disease. Her research has identified specific microbial signatures in early infancy that predict allergic outcomes years later, suggesting that intervention in the first months of life may be more consequential than later interventions.

The human immune system, gut barrier function, metabolic regulation, and even neurological development depend on the diverse microbial communities that historically inhabited and surrounded us. The mid-twentieth-century picture of microbes as primarily disease-causing organisms to be eliminated was substantially wrong. Most of our microbial neighbours are essential to our function.

IV. The Farm Effect

One of the more striking findings across allergy and asthma epidemiology is the protective effect of growing up on a farm. The effect has been documented across multiple European studies (GABRIELA, PARSIFAL, ALEX) and replicated in non-European contexts.

Erika von Mutius at the University of Munich has led much of this research. Her work has established that children growing up on traditional farms, particularly those with cattle and unprocessed milk, show substantially lower rates of asthma, hay fever, and atopic sensitisation than children in non-farming households in the same regions. The protective effect is dose-dependent: more time in the cowshed, more types of farm animals, and earlier exposure produce stronger protection.

The mechanism is now reasonably well characterised. Farm environments contain high levels of microbial diversity in dust, including bacteria, fungi, and bacterial cell wall components like endotoxin. Exposure to this microbial diversity during early development drives immune education in ways that urban environments cannot replicate. Markus Ege, von Mutius’s collaborator, has produced work identifying specific microbial signatures in farm dust associated with the protective effect.

The most striking demonstration of the farm effect comes from comparing two North American populations: the Amish of Indiana, who maintain traditional farming with close contact between humans and animals, and the Hutterites of South Dakota, who farm using modern industrialised methods with animals housed separately from humans. The two populations share German Swiss ancestry and similar dietary and lifestyle patterns in many respects. The asthma rate among Amish children is approximately 4%. The rate among Hutterite children is approximately 20%. The five-fold difference appears to be driven primarily by differences in environmental microbial exposure in early childhood.

The practical implication isn’t that everyone should move to a farm. It’s that the modern urban environment, with its sterile surfaces, minimal animal contact, and limited microbial diversity, represents a substantial departure from the conditions under which the human immune system evolved. Reintroducing some elements of microbial exposure (pets, gardens, soil contact, outdoor play) plausibly captures some of the protective effect.

V. The Karelia Studies and Biodiversity

A separate research line, led by Tari Haahtela at Helsinki University and colleagues, has compared populations divided by political accident across the Finnish-Russian border in Karelia. The two populations share genetic ancestry and historical culture but have lived under different political and economic conditions since the Soviet era. Finnish Karelia became part of a wealthy industrialised European nation; Russian Karelia remained substantially more agricultural and less industrialised, with lower hygiene standards and more environmental microbial exposure.

The findings: Russian Karelians show substantially lower rates of allergic disease, atopic sensitisation, asthma, and type 1 diabetes than Finnish Karelians despite genetic similarity. The differences correlate with measurable differences in environmental microbial diversity, skin microbial composition, and immune regulatory function.

Haahtela and colleagues have proposed a broader “biodiversity hypothesis” that extends Rook’s old friends framework. The argument: not only specific commensal microbes but the broader biodiversity of the environment, including plants, soil, animals, and the microbial communities associated with all of these, contributes to immune health. The collapse of biodiversity in modern industrialised environments may be implicated in the rise of inflammatory disease.

This connects the hygiene hypothesis to the broader picture of human-environment interaction covered in The Singularity. Humans evolved as parts of biodiverse ecosystems, and our biology assumes contact with that biodiversity. The modern reduction of biodiversity in our daily surroundings has health consequences beyond the obvious environmental ones.

VI. Early-Life Windows

The microbiome research has clarified that early-life microbial exposures are disproportionately consequential. Several specific moments in early development establish patterns that persist for years or decades.

• Birth canal vs C-section delivery: Maria Gloria Dominguez-Bello at NYU has documented that vaginally delivered infants acquire a microbiome dominated by maternal vaginal and gut bacteria, while C-section infants acquire one dominated by skin bacteria. The two profiles differ for months after birth, and C-section delivery is associated with elevated rates of asthma, allergies, type 1 diabetes, and obesity later in life. Dominguez-Bello’s group has explored “vaginal seeding” (swabbing C-section infants with maternal vaginal microbes immediately after birth) as a potential intervention, with mixed early results that warrant further research.
• Breastfeeding: Breast milk contains its own microbiome, prebiotic oligosaccharides that selectively feed beneficial gut bacteria (particularly Bifidobacterium), and immune factors that shape the developing immune system. Breastfeeding duration is associated with reduced rates of allergic and autoimmune disease in epidemiological studies, with the protective effect appearing dose-dependent.
• Antibiotic exposure in infancy: Broad-spectrum antibiotics in the first year of life have been associated with elevated rates of asthma, allergic disease, inflammatory bowel disease, and obesity later in childhood and adulthood. The effects appear stronger with earlier exposure and with multiple courses. This doesn’t mean antibiotics shouldn’t be used when genuinely needed. It means the threshold for use should be higher than it sometimes is in current pediatric practice.
• Daycare and sibling exposure: Confirming Strachan’s original observation, multiple studies have found that children attending daycare or having older siblings show reduced rates of allergic disease, particularly when exposure begins in the first year of life. The protective effect appears to operate through both microbial exposure and the immune challenge of childhood viral infections.
• Pet ownership: Children growing up in households with dogs, particularly outdoor or farm dogs, show reduced rates of allergic disease. The effect appears to be mediated through the diverse microbial communities that dogs bring into the home from the outdoor environment.

VII. The Dietary Dimension

The microbiome you maintain across adult life is shaped substantially by what you eat. The Sonnenburgs’ research and that of others have established that dietary fibre is the primary substrate for the diverse fermentative bacteria that populate a healthy gut microbiome.

The Western dietary pattern, characterised by low fibre intake, high refined sugar, high industrial seed oils, and limited plant diversity, produces a less diverse gut microbiome than traditional dietary patterns. The Sonnenburgs’ mouse research found that low-fibre diets caused progressive loss of microbial diversity across generations, with offspring inheriting depleted microbiomes from low-fibre-fed parents. Re-introducing fibre partially restored diversity in the original generation, but did not fully restore the lost species in subsequent generations.

The implications for adult practice:

• Eating a wide variety of plant foods, particularly fibrous vegetables, legumes, whole grains, and fruits, provides the substrate for diverse microbial communities.
• Fermented foods (yoghurt, kefir, sauerkraut, kimchi, miso, traditional unpasteurised cheeses where available and safe) provide both microbial diversity and metabolites that support gut function. A 2021 Stanford study by Sonnenburg, Christopher Gardner, and colleagues found that increasing fermented food intake increased microbiome diversity and decreased inflammatory markers, while increasing fibre alone did not produce the same effects in the short-term experiment.
• Highly processed foods, frequent antibiotic use, and chronic stress all reduce microbiome diversity.
• Plant diversity matters more than total quantity. The American Gut Project found that people eating more than 30 different plant species per week had substantially more diverse microbiomes than those eating fewer than 10.

VIII. What “Hygiene” Actually Means

The recurring confusion in popular discussion of the hygiene hypothesis is the assumption that “hygiene” in the technical sense means hand-washing, food safety, and sanitation. It doesn’t. Or at least, those aren’t the practices the hypothesis indicts.

What protects against allergic and autoimmune disease:

• Contact with diverse environmental microbes (soil, animals, outdoor environments)
• Early-life microbial exposure during the developmental window
• Diverse plant-rich diet supporting microbiome diversity
• Vaginal birth, breastfeeding, and minimal early antibiotic use where possible
• Exposure to siblings and other children

What doesn’t seem to harm immune development:

• Hand-washing before eating and after using the bathroom
• Cooking meat to safe temperatures
• Refrigerating perishable foods
• Cleaning surfaces that have contacted raw meat or other contamination sources
• Standard sanitation infrastructure (treated water, sewage systems)

The line that the evidence draws is between hygiene against pathogens and over-sterilisation that eliminates ancient microbial exposures. Hand-washing before eating prevents transmission of fecal-oral pathogens; it doesn’t deplete the protective old friends. Antibacterial soap with triclosan goes further than necessary, eliminating skin commensals and likely contributing to antibiotic resistance. The frequent use of antibacterial cleaners on home surfaces eliminates the diverse environmental microbes that would otherwise be present in dust and on common-touch surfaces. The combination of urban living, indoor work, antibiotic-treated meat, low-fibre processed diet, antibacterial personal products, and minimal outdoor or animal contact creates a sustained microbial poverty across the lifespan.

IX. The Line

For most people in industrialised nations, the dominant practical concerns aren’t getting cleaner. They’re getting back some of the microbial richness that modernity has stripped out.

For families with young children:

• Don’t sterilise everything. Toys, pacifiers, and floors don’t need to be antibacterial-treated. The mother who picks up a dropped pacifier and licks it before returning it to the baby is, against the popular framing, doing the right thing microbiologically; pacifiers cleaned this way are associated with lower allergy rates than those sterilised between uses.
• Allow contact with soil, sand, grass, and outdoor environments from infancy.
• If a pet is feasible, have one. Dogs in particular, especially those that go outside, bring beneficial microbial diversity into the home.
• Use antibiotics in children only when genuinely indicated. The medical literature increasingly supports watchful waiting for many ear infections and respiratory illnesses where antibiotics were previously routine.
• Encourage outdoor play in varied environments, including parks, woods, beaches, and farms when accessible.
• Don’t bathe young children every day unless needed. Skin microbial communities take time to establish and are disrupted by frequent washing with harsh products.

For adults:

• Eat a diverse plant-rich diet. Aim for variety in plant species across the week.
• Include fermented foods regularly.
• Get outside, ideally daily. Time in green and biodiverse environments has documented benefits beyond just microbial exposure.
• Garden if you can. Soil contact and the bacteria associated with it appear to have measurable mood effects in addition to immune effects.
• Have pets if practical and reasonable for your situation.
• Avoid antibiotic use when not genuinely needed. When you do need them, complete the course and consider probiotic support during and after.

Normal hygiene remains good practice:

• Wash hands before eating, after using the bathroom, and after handling raw meat.
• Cook foods to safe temperatures.
• Refrigerate perishables.
• Don’t share toothbrushes or other items that transmit pathogens.
• Get appropriate vaccinations.
• Manage food allergies and existing immune conditions with medical guidance.

The wellness movement’s “raw water and unwashed produce” position is not better than mainstream sanitation; pre-modern populations died of cholera and dysentery at substantially higher rates than modern populations. The other extreme of antibacterial everything and indoor-only sterilised existence has its own costs in immune dysregulation. The line in between, where you maintain real hygiene against pathogens while allowing the ancient microbial contacts your immune system needs, is where the evidence points.

X. Cross-Links

The microbiome and environmental exposure themes connect to multiple other sections of the manual.

The dietary dimension of microbial health is covered in Nutrition. The fibre, plant diversity, and fermented foods picture sits within the broader question of how dietary patterns shape physiology.

The outdoor and biodiversity exposure dimension is covered further in The Singularity, which addresses the broader human-as-open-system framing within the biosphere.

The practical interventions for daily environmental management are in Lifestyle Design, including the cleaning product recipes that maintain hygiene without resorting to antibacterial chemicals that would deplete commensal microbes.

The material on contested questions in environmental health, including the political economy of agricultural antibiotic use and the broader picture of environmental endocrine disruption, is in The Environmental Rabbit Hole.