Gut Reaction: The Surprising Power of Microbes - Ed Yong - Science - The Guardian

Gut reaction: the surprising power of microbes | Ed Yong | Science...
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Thursday 25 August 2016 06.00BST 9 Comments
So, whats in the thermos? I asked.

I was standing in a lift at Washington University in St Louis, with Professor Je Gordon
and two of his students, one of whom was holding a metal canister.
Just some faecal pellets in tubes, she said.
Theyre microbes from healthy children, and also from some who are malnourished.
We transplanted them into mice, explained Gordon, as if this was the most normal thing
in the world.
The lift doors opened, and I followed Gordon, his students, and the thermos of frozen
pellets into a large room. It was lled with rows of sealed chambers made of transparent
plastic. Peering inside one of these chambers, I met the eyes of one of the strangest
animals on the planet. It looked like just a mouse, and that is precisely why it was so
weird. It was just a mouse, and nothing more.
Almost every other animal on Earth, whether centipede or crocodile, atworm or
amingo, hippo or human, is a teeming mass of bacteria and other microbes. Each of
these miniature communities is known as a microbiome. Every human hosts a
microbiome consisting of some 39 trillion microbes, roughly one for each of their own
cells. Every ant in a colony is a colony itself. Every resident in a zoo is a zoo in its own
right. Even the simplest of animals such as sponges, whose static bodies are never more
than a few cells thick, are home to thriving microbiomes.
But not the mice in Gordons lab. They spend their entire lives separated from the
outside world, and from microbes. Their isolators contain everything they need:
drinking water, brown nuggets of chow, straw chips for bedding, and a white styrofoam
hutch for mating in privacy. Gordons team irradiates all of these items to sterilise them
before piling them into loading cylinders. They sterilise the cylinders by steaming them
at a high temperature and pressure, before hooking them to portholes in the back of the
isolators, using connecting sleeves that they also sterilise.
It is laborious work, but it ensures that the mice are born into a world without microbes,
and grow up without microbial contact. The term for this is gnotobiosis, from the
Greek for known life. We know exactly what lives in these animals which is nothing.
Unlike every other mouse on the planet, each of these rodents is a mouse and nothing
more. An empty vessel. A silhouette, unlled. An ecosystem of one.
Each isolator had a pair of black rubber gloves axed to two portholes, through which
the researchers could manipulate what was inside. The gloves were thick. When I stuck
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my hands in, I quickly started sweating.

I awkwardly picked up one of the mice. It sat snugly on my palm, white-furred and
pink-eyed. It was a strange feeling: I was holding this animal but only via two black
protrusions into its hermetically sealed world. It was sitting on me and yet completely
separated from me. When I had shaken hands with Gordon earlier, we had exchanged
microbes. When I stroked this mouse, we exchanged nothing.
The mouse seemed normal, but it was not. Growing up without microbes, its gut had not
developed properly it had less surface area for absorbing nutrients, its walls were
leakier, it renewed itself at a slower pace, and the blood vessels that supplied it with
nutrients were sparse. The rest of its body hadnt fared much better. Compared with its
normal microbe-laden peers, its bones were weaker, its immune system was
compromised, and it probably behaved dierently too. It was, as microbiologist Theodor
Rosebury once wrote, a miserable creature, seeming at nearly every point to require an
articial substitute for the germs [it] lacks.
The woes of the germ-free mouse vividly show just how invaluable the microbiome is.
Most of us still see microbes as germs: unwanted bringers of pestilence that we must
avoid at all costs. This stereotype is grossly unfair. Most microbes do not make us sick. At
worst, they are passengers or hitchhikers. At best, they are invaluable parts of our
bodies: not takers of life but its guardians. They help to digest our food, educate our
immune systems, protect us from disease, sculpt our organs, guide our behaviour, and
maintain our health. This wide-ranging inuence explains why the microbiome has, over
the last decade, become one of the hottest areas of biology, and why Gordon arguably
the most inuential scientist in the eld is so fascinated by it.
By studying our microbial companions, he is trying to unpick exactly how the
microbiome is connected to obesity and its polar opposite malnutrition. He is studying
which species of microbes inuence these conditions, and how they in turn are
inuenced by our diets, our immune systems, and other aspects of our lives. Ultimately,
he wants to use that knowledge to manipulate the microbial worlds within us to improve
our health.
e Gordon may be one of the most respected scholars of the human

microbiome, but he is also one of the hardest to get in touch with. It took me six
years of writing about his work to get him to answer my emails, so visiting his
lab was a hard-won privilege. I arrived expecting someone gru and remote.
Instead, I found an endearing and aable man with crinkly eyes, a kindly smile,
and a whimsical demeanour. As he walked around the lab, he called people
professor including his students. His aversion to the media comes not from
aloofness, but from a distaste for self-promotion. He even refrains from attending
scientic conferences, preferring to stay out of the limelight and in his laboratory.
Ensconced there, Gordon has done more than most to address how microbes aect our
health. But whenever I asked Gordon about his inuence, he tended to deect credit on
to students and collaborators past and present a roster that includes many of the elds
biggest stars. Their status testies to Gordons hes not just a king, but a king-maker,
too. And his gurehead status is all the more remarkable because long before the
microbiome crossed his mind, he was already a well-established scientist who had
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published hundreds of studies on how the gut develops in a growing human body.
In the 1990s, he started to suspect that bacteria inuence this process, but he was also
struck by how dicult it would be to test that idea. The gut contains thousands of
species of microbes. Gordon aimed to isolate parts of this daunting whole and examine it
under controlled conditions. He needed that critical resource that scientists demand but
biology withholds: control. In short, he needed germ-free mice and lots of them so he
bred them himself. He could load these rodents with specic microbes, feed them with
pre-dened diets, and do so again and again in controlled and repeatable conditions. He
could treat them as living bioreactors, in which he could strip down the baing
complexity of the microbiome into manageable components that he could
systematically study.
In 2004, Fredrik Bckhed, a member of Gordons team, used the sterile rodents to run an
experiment that would set the entire lab on a focused path one devoted to
understanding the connections between the microbiome, nutrition, and health. They
inoculated germ-free mice with microbes harvested from the guts of conventionally
raised rodents. Normally, the sterile rodents can eat as much as they like without putting
on weight, but this ability disappeared once their guts were colonised. They didnt start
eating any more food if anything, they ate slightly less but they converted more of
that food into fat and so put on more pounds.
Mouse biology is similar enough to that of human beings for scientists to use them as
stand-ins in everything from drug testing to brain research; the same applies to their
microbes. Gordon reasoned that if those early results apply to humans, our microbes
must surely inuence the nutrients that we extract from our food, and thus our body
weight. That was a powerful insight. We typically think of weight as a simple balance
between the calories we take in through food and those we burn through physical
activity. By contrast, the idea that multitudes of organisms in our bodies could inuence
that balance was outlandish at the time. People werent talking about it, says Gordon.
And yet, in 2004, team member Ruth Ley found another connection between microbes
and weight, when she showed that obese people (and mice) have dierent communities
of microbes in their guts. The most obvious dierence lay in the ratio of the two major
groups of gut bacteria the rmicutes and the bacteroidetes. Obese people had more
rmicutes and fewer bacteroidetes than their leaner counterparts. This raised an obvious
question: does extra body fat cause a relative increase in rmicutes or, more
tantalisingly, does the tilt make individuals fatter? Is the connection, as Gordon likes to
put it, causal or casual? The team couldnt answer that question by relying on simple
comparisons. They needed experiments.
Thats where Peter Turnbaugh came in. Then a graduate student in the lab, he harvested
microbes from fat and lean mice, and then fed them to germ-free rodents. Those that got
microbes from lean donors put on 27% more fat, while those with obese donors packed
on 47% more fat. It was a stunning result: Turnbaugh had eectively transferred obesity
from one animal to another, simply by moving their microbes across. It was an Oh my
God moment, said Gordon. We were thrilled and inspired.
These results showed that the guts of obese individuals contain altered microbiomes
that can indeed contribute to obesity, at least in some contexts. The microbes were
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perhaps harvesting more calories from the rodents food, or aecting how they stored
fat. Either way, it was clear that microbes dont just go along for the ride; sometimes,
they grab the wheel.
They can also turn it in both directions. While Turnbaugh showed that gut microbes can
lead to weight gain, others have found that they can trigger weight loss. Akkermansia
muciniphila, one of the more common species of gut bacteria, is over 3,000 times more
common in lean mice than in those genetically predisposed to obesity. If obese mice eat
it, they lose weight and show fewer signs of type 2 diabetes.
Gut microbes also partly explain the remarkable success of gastric bypass surgery a
radical operation that reduces the stomach to an egg-sized pouch and connects it
directly to the small intestine. After this procedure, people tend to lose dozens of
kilograms, a fact typically accredited to their shrunken stomachs. But as a side-eect,
the operation also restructures the gut microbiome, increasing the numbers of various
species, including Akkermansia. And if you transplant these restructured communities
into germ-free mice, those rodents will also lose weight.
The worlds media treated these discoveries as both salvation and absolution for anyone
who struggles with their weight. Why bother adhering to strict dietary guidelines when a
quick microbial x is seemingly around the corner? Fat? Blame the bugs in your guts,
wrote one newspaper. Overweight? Microbes might be to blame, echoed another.
These headlines are wrong. The microbiome does not replace or contradict other
long-understood causes of obesity; it is thoroughly entangled with them.
Another of Gordons students, Vanessa Ridaura, demonstrated this in 2013 by using
mice to stage battles between the gut microbes of lean and obese people. First, she
loaded these human microbial communities into two dierent groups of germ-free
rodents. Next, she housed the mice in the same cages. Mice readily eat each others
droppings and so constantly ll their guts with their neighbours microbes. When this
happened, Ridaura saw that the lean microbes invaded guts that were already
colonised by obese communities, and stopped their new hosts from putting on weight.
The opposite invasions never worked: the obese communities could never establish
themselves in the gut when the lean ones were already there.
Its not that the lean communities were inherently superior at taking hold in a mouses
gut. Instead, Ridaura had tipped the battles in their favour by feeding her mice with
plant-heavy chow. Plants contain a wide variety of complex bres, and microbe
communities from lean guts contain a wider range of bre-busting species than those
from obese guts. So, when the obese communities colonised lean guts, they found that
every morsel of bre was already being devoured.
By contrast, when the lean communities entered obese guts, they found a glut of
uneaten bre and ourished. Their success only evaporated when Ridaura fed the mice
with fatty, low-bre chow, designed to represent the worst extremes of the western diet.
Without bre, the lean communities couldnt establish themselves or stop the mice from
putting on weight. They could only inltrate the guts of mice that ate healthily. The old
dietary advice still stands, over-enthusiastic headlines be damned.
An important lesson emerged: microbes matter but so do we, their hosts. Our guts, like
all ecosystems, arent dened just by the species within them but also by the nutrients
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that ow through them. A rainforest isnt just a rainforest because of the birds, insects,
monkeys, and plants within it, but also because ample rain and sunlight fall from above,
and bountiful nutrients lurk in the soil. If you threw the forests inhabitants into a desert,
they would fare badly. Ridauras experiments emphasised that although the microbiome
can help to explain what makes us fat or lean, it oers no simple solutions. And thats
something the team learned a second time, by studying a very dierent condition, in a
very dierent part of the world.
alawi has among the highest rates of child mortality in the world, and
half of these deaths are due to malnourishment. One form of
malnourishment, known as kwashiorkor, is especially severe and hard
to treat. From an early age, a childs uids leaks from their blood
vessels, leading to puy swollen limbs, distended stomachs, and
damaged skin.
Kwashiorkor has long been shrouded in mystery. It is said to be caused by protein-poor

diets, but how can that be when children with kwashiorkor often dont eat any less
protein than those with marasmus, another form of severe malnutrition? For that matter,
why do these children often fail to get better despite eating protein-rich food delivered
by aid organisations? And why is it that one child might get kwashiorkor while their
identical twin, who shares all the same genes, lives in the same village, and eats the
same food, gets marasmus instead?
Gordon thinks that gut microbes are involved, and might explain the dierences in
health between children who, on paper, look identical. After his team carried out their
groundbreaking obesity experiments, he started to wonder: if bacteria can inuence
obesity, could they also be involved in its polar opposite malnutrition? Many of his
colleagues thought it unlikely but, undeterred, Gordon launched an ambitious study. His
team went to Malawi and collected regular stool samples from infants until the age of
three; some had kwashiorkor, while others were healthy.
The team found that babies with kwashiorkor dont go through the same progression of
gut microbes as their healthy counterparts. Typically, these microbial communities
change in the rst years of life, in dramatic but predictable ways. Just as new islands are
rst colonised by lichens, then shrubs, then trees, so too is the infant gut colonised by
waves of species that arrive in standardised patterns. But in kwashiorkor infants,
microbiomes fail to diversify and mature correctly. Their inner ecosystems become
stagnant. Their microbiological age soon lags behind their biological age.
When Gordons team transplanted these immature communities from children with
kwashiorkor into germ-free mice, the rodents lost weight but only if they also ate chow
that mirrored the nutrient-poor Malawian diet. If the mice ate standard rodent chow,
they didnt lose much weight, no matter whose bacteria they were carrying. It was the
combination of poor food and the wrong microbes that mattered. The kwashiorkor
microbes seemed to interfere with chemical chain reactions that fuel our cells, making it
harder for children to harvest energy from their food food that contains very little
energy to begin with.
The standard treatment for malnutrition is an energy-rich, fortied blend of peanut
paste, sugar, vegetable oil and milk. But Gordons team found that the paste only has a
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brief eect on the bacteria of children with kwashiorkor (which perhaps explains why it
doesnt always work). As soon as they reverted to their normal Malawian diet, their
microbes also boomeranged back to their earlier impoverished state. Why?
All ecosystems have a certain resilience to change, which must be overcome to push
them into a dierent state. Thats true for coral reefs, rainforests, grassland and a
childs gut. A poor diet could change the microbes within the gut. The dietary
deciencies could also impair the childs immune system, changing its ability to control
the gut microbiome, and opening the door to harmful infections that alter the gut
communities even further. These communities could themselves start to harm the gut,
stopping it from absorbing nutrients eciently and leading to even worse malnutrition,
more severe immune problems, more distorted microbiomes, and so on.
This is what microbiome scientists call dysbiosis a state where the entire microbial
community shifts into a harmful conguration. None of its members causes disease in its
own right; instead, the entire community is at fault. Its not clear exactly why the
microbiomes of malnourished infants stall in their development in the rst place. There
are many possible reasons including antibiotic exposures, gut diseases, and poor diets,
which vary from person to person. Whats clearer is that once microbiomes end up in a
dysbiotic state, it can be hard to pull them back.
But Gordon is trying. His student Laura Blanton, the same woman who I met carrying
that thermos of mouse droppings in the lift, recently implanted mice with microbes from
either healthy infants or underweight ones. She then housed rodents from both groups
in the same cages, allowing them to swap their microbiomes. When they did so, the
normal communities from the healthy infants invaded and displaced the immature
communities from the malnourished ones.
Blanton found that ve species of bacteria from the healthy microbiomes were
especially good at colonising the immature ones. When she fed this quintet to mice
carrying the microbiomes of malnourished children, the rodents put on weight in a
normal, healthy way. Rather than breaking down the amino acids in their diet for energy,
they instead converted these nutrients into esh and muscle.
This promising experiment suggests that the team might be able to create a probiotic
cocktail of specially chosen bacteria that can turn a dysbiotic gut into a healthy one. But
theres reason to be cautious. Despite the hype that surrounds them, current probiotics
products that contain supposedly benecial microbes confer few big health benets,
because they contain small amounts of bacteria and consist of strains that are bad at
taking hold in the gut. Gordon knows that if he wants to concoct better products, he
must nd ways of giving the incoming microbes a competitive advantage in their new
homes. Maybe that means pairing the probiotics with foods that will nourish them.
Maybe it means treating the human hosts as well as the microbes they carry, or training
their immune systems to accept the newcomers.
Gordon is optimistic but cautious. As he sees it, studying the microbiome will ultimately
help us to better treat conditions that are still mysterious and often intractable. But as he
has said to me on more than one occasion, hes wary of the intense hype that clouds the
microbiome world. I talk about the importance of sobriety and humility, he says.
Theres lots of hope and expectation around this transcendent view of ourselves. But
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he and other microbiome researchers still need to show that their discoveries can help
people.
iscoveries by Gordon and others have created the perception that the
microbiome is the answer to everything. It has been linked to an absurdly
long list of conditions that includes Crohns disease, ulcerative colitis,
irritable bowel syndrome, colon cancer, type 1 diabetes, type 2 diabetes,
coeliac disease, allergies, atherosclerosis, autism, asthma, Alzheimers
disease, Parkinsons disease, multiple sclerosis, depression, anxiety,
rheumatoid arthritis, stroke, and many more.
Many of these proposed links are just correlations. Researchers often compare people
with a particular disorder to healthy volunteers, nd microbial dierences, and stop.
Those dierences hint at a relationship but they dont reveal its nature or its direction.
Studies by Gordon and others go one step further. By showing that transplanted
microbes can reproduce health problems in germ-free mice, they strongly hint at a
causal eect.
Still, they provide more questions than answers. Did the microbes set symptoms in
motion or just make a bad situation worse? Was one species responsible, or a group of
them? Is it the presence of certain microbes that matters, or the absence of others, or
both? And even if experiments show that microbes can cause diseases in mice and other
animals, we still dont know if they actually do so in people. Beyond the controlled
settings of laboratories and the atypical bodies of lab rodents, are microbial changes
really aecting our everyday health? When you enter the messy, multifaceted world of
dysbiosis, the lines of cause and eect become much harder to untangle.
There is still a lot about the microbiome that we do not understand, and some of what
we think we know is almost certainly wrong.
Remember how obese people and mice have more rmicutes and fewer bacteroidetes in
their guts than their lean counterparts? This famous nding worked its way into the
mainstream press and the scientic literature and its a mirage. In 2014, two attempts
to re-analyse past studies found that the F/B ratio is not consistently connected to
obesity in humans. This doesnt refute a connection between the microbiome and
obesity. You can still fatten germ-free mice by loading them with microbes from an obese
mouse (or person). Something about these communities aects body weight; its just not
the F/B ratio, or at least not consistently so.
It is humbling that, despite a decade of work, scientists are barely any closer to
identifying microbes that are clearly linked to obesity, which has received more
attention from microbiome researchers than any other. I think that everybody is
coming to the realisation that, unfortunately, a really compelling simple biomarker, like
the percentage of a certain microbe, is not going to be enough to explain something as
complicated as obesity, said Katherine Pollard, who led one of the re-analyses.
These conicting results naturally arise in the early days of a eld because of tight
budgets and imprecise technology. Researchers run small, exploratory studies
comparing handfuls of people or animals in hundreds or thousands of ways. The
problem is that they end up being like the Tarot, said Rob Knight, another leading
microbiome scientist. You can tell a good story with any arbitrary combination.
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Human geneticists faced the same problem. In the early 21st century, when technology
hadnt quite caught up with ambition, they identied many genetic variants that were
linked to diseases, physical traits, and behaviours. But once sequencing technology
became cheap and powerful enough to analyse millions of samples, rather than dozens
or hundreds, many of these early results turned out to be false positives. The human
microbiome eld is going through the same teething problems.
It doesnt help that the microbiome is so variable that the communities in lab mice can
dier if they belong to dierent strains, come from dierent vendors, were born to
dierent mothers, or were reared in dierent cages. These variations could account for
phantom patterns or inconsistencies between studies. There are also problems with
contamination. Microbes are everywhere. They get into everything, including the
chemical reagents that scientists use in their experiments. But these problems are now
being ironed out. Microbiome researchers are getting increasingly savvy about
experimental quirks that bias their results, and theyre setting standards that will shore
up the quality of future studies. They are calling for experiments that will show
causality, and tell us how changes in the microbiome lead to disease. They are looking at
the microbiome in even greater detail, moving towards techniques that can identify the
strains within a community, rather than just the species.
They are also setting up longer studies. Rather than capturing a single screenshot of the
microbiome, they are trying to watch the entire movie. How do these communities
change with time? What makes them resilient or unstable? And does their degree of
resilience predict a persons risk of disease? One team is recruiting a group of 100
volunteers who will collect weekly stool and urine samples for nine months, while
eating specic diets or taking antibiotics at xed times. Others are leading similar
projects with pregnant women (to see if microbes contribute to pre-term births) and
people at risk of developing type 2 diabetes (to see if microbes aect their progression to
full-blown disease).
And Gordons group has been charting the normal progression of microbes in healthy
developing babies, and how it stalls in kids with kwashiorkor. Using stool samples
collected from Bangladeshi and Malawian children over their rst two years, the team
has created a score that measures the maturity of their gut communities and will
hopefully predict if symptomless infants are at risk of developing kwashiorkor. The
ultimate goal of all of these projects is to spot the signs of disease as early as possible,
before a body turns into the equivalent of an algal reef or a fallow eld: a degraded
ecosystem that is very hard to repair.
rofessor Planer! said Je Gordon. How are you? He meant Joe

Planer, one of his students, who was standing in front of a standard
laboratory bench, complete with pipettes, test tubes and Petri dishes,
all of which had been sealed in a transparent, plastic tent. It looked like
one of the isolators from the germ-free facility but its purpose was to
exclude oxygen rather than microbes. It allowed the team to grow the
many gut bacteria that are extremely intolerant of the gas. If you write the word oxygen
on a piece of paper and show it to these bugs, theyll die, said Gordon.
Starting o with a stool sample from a Malawian child with kwashiorkor, Planer used the
anaerobic chamber to culture as many of the microbes within it as possible. He then
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picked o single strains from these collections, and grew each one in its own
compartment. He eectively turned the chaotic ecosystem within a childs gut into an
orderly library, dividing the teeming masses of microbes into neat rows and columns.
We know the identity of the bacteria in each well, he said. Well now tell the robot
which bacteria to take and combine in a pool.
He pointed to a machine inside the plastic, a mess of black cubes and steel rods. Planer
can programme it to suck up the bacteria from specic wells and mix them into a
cocktail. Grab all the Enterobacteriaceae, he might say, or all the Clostridia. He can then
transplant these fractions back into germ-free mice to see if they alone can confer the
symptoms of kwashiorkor. Is the whole community important? Will the culturable
species do? A single family? A single strain? The approach is both reductionist and
holistic. Theyre breaking down the microbiome, but then recombining it. Were trying
to work out which actors are responsible, said Gordon.
A few months after I saw Planer working with the robot, the team had narrowed down
the kwashiorkor community to just 11 microbes that replicate many of the diseases
symptoms in mice. None of these were harmful on their own. They only caused a
problem when acting together and even then, only when the mice were starved of
nutrients. The team also created culture collections from healthy twins who didnt
develop kwashiorkor, and identied two bacteria that counteract the damage inicted by
the deadly 11. The rst is Akkermansia, which is being studied as a way of reducing body
weight, but seemingly guards against malnutrition too. The second is Clostridium
scindens, which tamps down inammation by stimulating certain branches of the
immune system.
Opposite the tented bench, there was a blender that could take foods representative of
dierent diets and pulverise them into rodent-friendly chow. (On a piece of sticky tape,
axed to the blender, someone had written Chowbacca.) Gordons lab could now
explore the behaviour of Akkermansia and C scindens, either in test tubes or in the
gnotobiotic mice, and work out which nutrients the microbes needed. This allowed the
team to compare the eects of the same microbes when fed a Malawian diet, or an
American one, or on sugars from breast milk that have specically evolved to feed
benecial microbes. Which of these foods works best? And which genes do the microbes
switch on? The team can take any one microbe and create a library of thousands of
mutants, each of which contains a broken copy of a single gene. They can put these
mutants in a mouse to see which genes are important for surviving in the gut, liaising
with other microbes, and both causing or protecting against kwashiorkor.
What Gordon has built is a causality pipeline a set of tools and techniques that, he
hopes, will more conclusively tell us how our microbes aect our health, and take us
from guesswork and speculation to actual answers. Kwashiorkor is just the start. The
same techniques could work for any disease with a microbial inuence.
It is the right time to be doing this work. Our planet has entered the Anthropocene a
new geological epoch when humanitys inuence is causing global climate change, a loss
of wild spaces, and a drastic decline in the richness of life. Microbes are not exempt.
Whether on coral reefs or human guts, we are disrupting the relationships between
microbes and their hosts, often pulling apart species that have been together for millions
of years. Gordon is working hard to understand these partnerships to better forestall
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their untimely end. He is not just a scholar of the microbiome; he is one of its stewards.
M a i n p h o t o g ra p h o f f a e c a l b a c t e r i a : S c i e n c e P h o t o L i b ra r y
This is an edited extract from I Contain Multitudes, published by Bodley Head
Follow the Long Read on Twitter at @gdnlongread, or sign up to the long read weekly
email here.
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Thursday 25 August 2016 06.00BST 9 Comments

So, whats in the thermos? I asked.