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How Burgers and Fries Are Killing Your Microbial Balance

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Did the American diet kill our ancestral microbiome? If so, can we repair it?

Wow, the differences in microbiomes are HUGE.

A group of Italian microbiologists had compared the intestinal microbes of young villagers in Burkina Faso with those of children in Florence, Italy. The villagers, who subsisted on a diet of mostly millet and sorghum, harbored far more microbial diversity than the Florentines, who ate a variant of the refined, Western diet. Where the Florentine microbial community was adapted to protein, fats, and simple sugars, the Burkina Faso microbiome was oriented toward degrading the complex plant carbohydrates we call fiber.

Scientists suspect our intestinal community of microbes, the human microbiota, calibrates our immune and metabolic function, and that its corruption or depletion can increase the risk of chronic diseases, ranging from asthma to obesity. One might think that if we coevolved with our microbes, they’d be more or less the same in healthy humans everywhere. But that’s not what the scientists observed.

We are killing good microbiota with a fiber-poor diet.

How did the microbiome of our ancestors look before it was altered by sanitation, antibiotics, and junk food?

Indeed, when Sonnenburg fed mice plenty of fiber, microbes that specialized in breaking it down bloomed, and the ecosystem became more diverse overall. When he fed mice a fiber-poor, sugary, Western-like diet, diversity plummeted. (Fiber-starved mice were also meaner and more difficult to handle.) But the losses weren’t permanent. Even after weeks on this junk food-like diet, an animal’s microbial diversity would mostly recover if it began consuming fiber again.

This was good news for Americans—our microbial communities might re-diversify if we just ate more whole grains and veggies. It was bad news, however, that the Western diet had triggered microbial extinctions. They saw what happened when pregnant mice went on the no-fiber diet: temporary depletions became permanent losses.

When we pass through the birth canal, we are slathered in our mother’s microbes, a kind of starter culture for our own community. In this case, though, pups born to mice on American-type diets—no fiber, lots of sugar—failed to acquire the full endowment of their mothers’ microbes. Entire groups of bacteria were lost during transmission. When Sonnenburg put these second-generation mice on a fiber-rich diet, their microbes failed to recover. The mice couldn’t regrow what they’d never inherited. And when these second-generation animals went on a fiberless diet in turn, their offspring inherited even fewer microbes. The microbial die-outs compounded across generations.

Many who study the microbiome suspect that we are experiencing an extinction spasm within that parallels the extinction crisis gripping the planet. Numerous factors are implicated in these disappearances. Antibiotics, available after World War II, can work like napalm, indiscriminately flattening our internal ecosystems. Modern sanitary amenities, which began in the late 19th century, may limit sharing of disease- and health-promoting microbes alike. Today’s houses in today’s cities seal us away from many of the soil, plant, and animal microbes that rained down on us during our evolution, possibly limiting an important source of novelty.

But what the Sonnenburgs’ experiment suggests is that by failing to adequately nourish key microbes, the Western diet may also be starving them out of existence. They call this idea “starving the microbial self.” They suspect that these diet-driven extinctions may have fueled, at least in part, the recent rise of non-communicable diseases. The question they and many others are now asking is this: How did the microbiome of our ancestors look before it was altered by sanitation, antibiotics, and junk food? How did that primeval collection of human microbes work? And was it somehow healthier than the one we harbor today?

The Sonnenburgs think fiber is so important that they’ve given it a new designation: microbiota-accessible carbohydrates, or MACs. 

They think that the mismatch between the Westernized, MAC-starved microbiome and the human genome may predispose to Western diseases.


When I visited Sonnenburg, he showed me one reason why: The ecosystem that produces the acids may be as important as the acids themselves. He brought up two cross-sectional images of fecal pellets still in mice intestines. Most microbiome analyses take a tally, from genetic markers, of what microbes are present and in what abundance. That’s equivalent to imagining what a forest looks like from a pile of wood chips, and gives little sense of how the forest was organized. By some ingenious tinkering, though, one of Sonnenburg’s post-docs had developed a way to freeze the ecosystem in place, and then photograph it.

The resulting picture was unlike any rendition of the microbiome I’d seen before. One animal had eaten plenty of fiber, the other hadn’t. In the fiber-fed ecosystem, similar bacteria clustered with one another, not unlike schools of fish on a reef ecosystem. An undulating structure prevailed across space. But in the non-fiber diet, not only was diversity reduced, the microbes were evenly distributed throughout, like a stew boiled for too long.

At this point, Sonnenburg sat back in his chair and went quiet, waiting for me to notice something. To one side of both images, microbes were mostly absent—the mucus layer on the lining of the gut. But that layer was twice as thick in the fiber-fed mice than the non-fiber fed. That difference amounted to about 30 nanometers, far less than the width of a human hair. But one day we may look back and shake our heads that Western diseases—from diabetes to colon cancer—stemmed from 30 nanometers of mucus that, somewhere along the way, went missing in the developed world.

We think of the Western diet—high in unhealthy fats, sugar, and proteins—as overly rich. But what’s missing from the diet may be just as, and perhaps more, important than what’s abundant.

Years ago, while still a post-doc, Sonnenburg discovered that something very odd occurs when those MAC-loving microbes go hungry. They start eating mucus. “This is the stage where you say, ‘Oh my God. They’re eating me.’ ” Sonnenburg said. “You can see it.”

Our ancestral microbe variety may have faded over time due, simply, to our fiber-poor diet.

We need that mucus. It maintains a necessary distance between us and our microbes. And as it erodes with a poor diet, the lining of the gut becomes irritated. Microbial detritus starts leaking through. One of the more striking discoveries in recent years is that you can see this stuff, called endotoxin, increase in the bloodstream immediately after feeding people a sugary, greasy, fast-food meal. The immune system responds as if under threat, leading to the “simmering inflammation” the Sonnenburgs think drives so many Western diseases.

We need inflammation to combat infections, or aid tissue repair. But chronic inflammation—a danger signal blaring indefinitely—can lead to all manner of cellular dysfunction, contributing to many degenerative diseases.

I came away from Sonnenburg’s office with a sense that I’d glimpsed a principle underlying our relationship with microbes. Wringing calories from wild, fibrous fare required a village—microbes specialized in distinct tasks, but each also dependent on its neighbors. The difficulty of the job encouraged cooperation between microbes. When you withheld fiber, though, you removed the need for that close-knit cooperation. The mutually beneficial arrangements began to fray.

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