You are what you eat – how your diet defines you in trillions of ways

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We depend on a special organ to digest the food we eat and you won’t find it in any anatomy textbook. It’s the ‘microbiome’ – a set of trillions of bacteria living inside your intestines that outnumber your own cells by ten to one. We depend on them. They wield genes that allow them to break down molecules in our food that we can’t digest ourselves. And we’re starting to realise that this secret society within our bowels has a membership roster that changes depending on what we eat.

These changes take place across both space and time. Different cultures around the world have starkly contrasting diets and their gut bacteria are different too. As we grow older, we eat increasingly diverse foods, from the milk of infancy to the complex menus of adulthood. As our palate changes, so do our gut bacteria.

It all starts from the moment we’re born, when we inherit our first microbiome from our mums – a zeroeth birthday present that give us the digestive abilities that we need from day one. These first colonists are laden with genes for digesting milk proteins, allowing babies to make full use of their only source of nourishment.

But breast milk isn’t just a meal for baby, but for baby’s first gut bacteria. After lactose and fat, the third most common ingredients in breast milk are small sugar molecules called ‘oligosaccharides’. Gut bacteria thrive on these and Angela Zivkovic from the University of California, Davis thinks that they evolved as part of breast milk, to selectively feed the right bacteria in a baby’s bowels.

Breast milk contains over 200 types of oligosaccharides. They’re part of a baby’s immune system by acting as decoys for disease-causing bacteria. They look like molecules on the surface of human cells, which infectious bacteria recognise and stick to. By presenting alternative targets, the oligosaccharides divert these bacteria away from actual cells.

But they also feed helpful bacteria just as they distract harmful ones. The bifidiobacteria, which are common in the guts of breast-fed infants, have a preference for milk oligosaccharides, and some species can survive on these molecules alone. So when mum suckles her infant, she’s looking after both her baby and its partners-in-digestion.

Of course, babies  are eventually weaned off milk and as they move to solid foods, their guts are the sites of tumultuous change. Jeremy Koenig from Cornell University studied these shifts by tracking the gut bacteria of one specific baby for its first 2.5 years. Koenig had the unenviable task of collecting over 60 samples from the baby’s soiled diapers. As the child grew up, the bacteria in his guts became gradually more diverse, but the roster went through four bigger shifts all associated with big life events – getting fever, starting on solid foods, taking antibiotic treatments, and shifting from breast milk to cow milk.

With each change, the baby’s microbiome started wielding different genetic tools. His first group were rife with genes for digesting milk proteins. Just before he was weaned on solid food, his microbiome started activating genes that break down the complex sugars and starches in plant food. It was already prepared for the arrival of peas and other table food. And when he actually started eating these foods, the bacteria changed even further to include more members of the Bacteroidetes, a family that specialises in digesting plant molecules.

In the baby’s second year, when he started scoffing increasingly complex foods, the abilities of his microbiome diversified again. They started activating genes that can use carbohydrates effectively, produce vitamins, and break down unusual and diverse chemicals. Koenig thinks that things settle down at this point and the make-up of our bacterial cartel becomes relatively stable. Even after an antibiotic assault, the same species bounce back in the same numbers. But once again, the food we eat determines which species set up shop in the first place.

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Carlotta de Filippo compared the gut bacteria of 14 children from a village in Burkina Faso with those of 14 children in Florence, Italy. The African children came from families of subsistence farmers and their menus were mostly vegetarian. The eat little in the way of fat or animal protein and their diet is heavy in fibre, starch and plant carbohydrates. By contrast, the Italian kids ate a typical Western diet, high in animal protein, sugar, starch and fat and low in fibre. They ate about half as much fibre as their African peers and about 50% more calories.

These differences are reflected in their bowels. The bacterial community in the African guts were dominated by those plant-digesting specialists, the Bacteroidetes. They probably helped the children to break down the tough fibres that they eat and extract more energy from their meals. Meanwhile, the Italian bowels were dominated by another group, the Firmicutes, which are generally more common in obese people compared to lean ones.

Of course, diet is just one of many traits that separate children from Italy and Burkina Faso, including genes, hygiene and climate. But the youngest babies in de Filippo’s sample show that diet wields by far the greatest influence on the microbiome. The toddlers, unlike their older peers, all ate the same food – breast milk – and as a result, their microbiomes were very similar to one another’s, despite the gulf of differences between their cultures. It’s only at the point of weaning when their diets diverged that their gut communities did too.

The African children also had a greater diversity of gut bacteria, which probably hitch a ride into their bodies via their food. In Europe, generic, uncontaminated food presents a blockade to bacteria from the outside world, which means that Western gut communities have become gentrified. They lack genetic diversity, and they have few ways of increasing it.

This is bad news, for bacteria from the outside world provide a reservoir of useful genes that could help the microbiome to adapt to unusual diets. The fibre-digesting abilities of the Burkina Faso children are probably one example of this. A more striking one was discovered just last year: Japanese gut bacteria have borrowed genes from an oceanic species, which allow them to digest carbohydrates in seaweed. Western diets hold back this evolutionary potential.

But De Filippo thinks that the problems are bigger. An unbalanced or simplified microbiome could be damaging the health of Westerners more directly, affecting the risk of a variety of other medical conditions, including allergies, inflammatory bowel disease, bowel cancer and obesity. A diverse microbiome could also prevent more harmful species from setting up shop – indeed, and somewhat unexpectedly, food poisoning bacteria like Shigella and Escherichia were less common in the Burkinabe children than the Italian ones.

As we learn more about our bacterial partners, we might eventually find ways of influencing them to improve our health, just as breast milk appears to selectively nourish helpful species. The prospect of combating obesity, allergies or infections by inoculating people with the right bacteria might seem far-fetched but it’s already happening. In 2008, Alexander Khoruts from the University of Minnesota managed to cure a woman with a “vicious gut infection” by giving her a transplant of her husband’s gut bacteria.

A success like this is just the beginning, based on a fairly limited understanding of the microbiome. Koenig’s study demonstrates how important it is to look at gut bacteria over time while de Filippo shows that it’s equally essential to look at how they vary from place to place. This is the sort of deeper understanding that future triumphs will be built from.

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