Westernization and Skin: Which Microbes Did We Lose When We Moved Indoors?

The Hadza people of Tanzania spend most of their waking hours outside, digging tubers with bare hands, collecting honey from wild hives, sleeping near open fires. When researchers swabbed their skin in 2018, they found bacterial communities that looked nothing like those of urban Westerners—richer in environmental species, more diverse overall, and notably abundant in microbes we now consider rare. The question wasn't what the Hadza had gained, but what the rest of us had lost.

What disappeared when we closed the windows?

Industrialization didn't just change where we live. It changed what lives on us. The shift happened in stages: indoor plumbing in the late 1800s, widespread soap use by the 1920s, air conditioning in the 1950s, antibacterial everything by the 1990s. Each innovation distanced us from environmental microbes—the ones that blow in on wind, live in soil, colonize our skin from plants and animals and dust.

A landmark 2012 survey of belly button bacteria found that people who spent more time outdoors harbored more diverse microbial communities, including species rarely seen on indoor-dwelling urbanites. Some of these environmental colonizers—Pseudomonas, Acinetobacter, certain Bacillus strains—likely played roles we're only beginning to understand: training the immune system, competing with pathogens, even producing compounds that modulate inflammation.

We didn't just reduce microbial exposure. We replaced it. Synthetic fabrics, sealed buildings, daily showering, preservative-laden cosmetics—all of these favored different microbes. The ones that survived the new regime were those that could thrive in a low-moisture, nutrient-poor, chemically hostile environment.

Which species thrived in the new normal?

Not all bacteria suffered under Westernization. Cutibacterium acnes, which lives deep in sebaceous follicles, did just fine—protected from soap and sanitizer by the very oil glands it feeds on. Staphylococcus epidermidis adapted too, clinging to the skin's surface even after aggressive cleansing. Malassezia fungi, which metabolize the oils we produce, actually became more dominant as other competitors disappeared.

But diversity collapsed. Studies comparing rural populations in the Amazon, Papua New Guinea, and sub-Saharan Africa to urban Americans consistently find the same pattern: Western skin hosts fewer species overall, with a handful of oil-loving, desiccation-tolerant microbes accounting for most of the biomass. We didn't eliminate our microbiome. We streamlined it. (For more on how modern exposures continue to shape microbial communities, see our exploration of pollution and the skin microbiome.)

The losers were the transient environmental species—the ones that would have wandered onto our skin from soil, water, vegetation, and animals, then wandered off or been outcompeted. These weren't permanent residents, but their absence may matter more than we thought.

What did those lost microbes actually do?

We don't have a complete answer, but clues are emerging. Some environmental bacteria produce metabolites that dampen inflammatory signaling—essentially coaching the skin's immune system to distinguish harmless visitors from real threats. Others secrete enzymes that break down environmental toxins or compete with pathogenic species for space and nutrients.

Research from the Gallo lab has shown that certain Staphylococcus strains produce antimicrobial peptides that actively inhibit Staphylococcus aureus, a pathogen linked to eczema and skin infections. Many of these protective strains are more common in people with high environmental microbial exposure. When that exposure drops, so does microbial-mediated defense.

The hypothesis gaining traction: we didn't just lose individual species. We lost ecological functions—nutrient cycling, immune education, pathogen resistance—that depended on a richer, more dynamic microbial community.

Why this matters for your skin

The Westernization of the skin microbiome may help explain why inflammatory skin conditions—eczema, rosacea, seborrheic dermatitis—have risen sharply in industrialized nations over the past century. Rebuilding diversity doesn't mean abandoning hygiene, but it might mean rethinking the scorched-earth approach to cleansing and rethinking how much time we spend in completely sterile environments (for a deeper look at this balance, see what happens to your skin microbiome in sealed indoor spaces).

References

• Nakatsuji T, Hata TR, Tong Y, Cheng JY, Shafiq F, Butcher AM, et al. Development of a human skin commensal microbe for bacteriotherapy of atopic dermatitis and use in a phase 1 randomized clinical trial. Nature medicine. 2021.
• Byrd AL, Belkaid Y, Segre JA. The human skin microbiome. Nat Rev Microbiol. 2018.
• Nakatsuji T, Chen TH, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis. Sci Transl Med. 2017.
• Prescott SL, Larcombe DL, Logan AC, et al. The skin microbiome: impact of modern environments on skin ecology, barrier integrity, and systemic immune programming. World Allergy Organ J. 2017.
• Oh J, Byrd AL, Deming C, et al. Biogeography and individuality shape function in the human skin metagenome. Nature. 2014.