By Simon Cork, Neurophysiologist, Imperial College London, @SimonCorkPhD
You may have heard many scientists and media types getting excited over the term “microbiome” recently. There was a series on BBC Radio 4 termed “The Second Genome” recently dedicated to it, and a succession of articles on the BBC News website 1 2. But what exactly is it, what does it do, and should we all be excited?
The microbiome is the term scientists give the community of bacteria that live in your guts (micro meaning small, and biome meaning biological community). People have been studying the microbiome for many years, and there is a remarkable amount of literature around the microbiome of insects. But recently, the microbiome of humans, and specifically the effects our microbiomes have on our overall health, has entered the spotlight.
In insects and other animals, the bacteria that live in and around them have remarkable effects not only on their heath but on their development. For many insects and animals, interactions with bacteria are a requirement for their survival. One particularly powerful example of the influence of bacteria on a host’s behaviour is in the fruit fly.
Feeding fruit flies different diets (and thus altering their gut microbiome composition) causes them to preferentially mate with flies fed on the same diet. When given antibiotics, which wipe out their bacteria, this preference disappears.
In humans, we are only just beginning to understand (or perhaps recognise) the importance that the microbiome has on our health. We are also beginning to understand how changes in our microbiome predispose, or even cause, certain diseases.
Less bacteria, more weight?
Take obesity for example. Worldwide, over 2.1 billion people are overweight or obese. The causes of obesity vary from person to person, but one common factor found in obese individuals is the lack of diversity of their gut bacteria. In a lean individual, the gut bacteria will contain a variety of different strains and species of bacteria. However, in individuals with obesity, this diversity is significantly reduced (with an increase in the ratio of the Firmicutes and a decrease in the Bacteoridates species).
We also know that babies who are born via caesarean section are at a higher risk of developing a number of health conditions in later life, one of which is obesity. The reasons why are not completely understood, but we know that C-section babies do not get the full complement of bacteria that babies born naturally get.
Essentially, in the first few months of life, a baby born via C-section has a gut bacterial population that more closely resembles that found on the skin, as this is often the first bacteria that they come into contact with.
Quite astonishingly, it may be possible that gut bacterial populations that predispose to disease act as a form of non-genetic inheritance of disease. For example, an obese mother, who likely has a bacterial population with a low diversity, may pass this low diversity to her child during delivery, thus predisposing them to obesity in later life.
So what does this mean? Well, the honest answer is we don’t quite know. At the moment, these observations are simply that, observations. We can predict whether or not a person will be obese or lean with 90% accuracy simply by studying the diversity of their microbiome, but what we don’t fully understand is how the bacteria are contributing to weight gain.
What’s in it for them: bacteria causing obesity? And other diseases?
One theory is that certain bacteria have the ability to harvest energy from our diets more effectively than others. Couple this with a sedentary lifestyle and you have the recipe for weight gain.
Another theory is that the bacteria are interfering with our brain chemistry. We know that many species of bacteria can secrete molecules that are either the same or have very similar chemistry to many of the molecules found in our brain, and we know that bacteria are able to secrete these chemicals in response to certain foods.
Could it be then, that our bacteria are driving our food choices? Imagine a population of gut bacteria that have a penchant for sugar; they use this as their main source of energy and want to make sure that it keeps coming. Is it possible that in response to their host eating a sugary meal, the bacteria release chemicals that tells their brain to eat more? This may sound far-fetched, but there’s increasing evidence that this may actually be happening.
There’s also increasing evidence that our gut bacteria may be driving a number of other conditions, including asthma, depression and anxiety, possibly through chemicals they release which interfere with our normal brain chemistry.
To each their own: individual differences and possible ways to shift them
So what can we do about this? Well, the bad news is this area of research is still very much in its infancy.
There are a few things we do know.
Our gut bacterial populations vary considerably from person to person, which makes a one-size fits all approach to fixing a dysfunctional microbiome tricky (although the microbiomes of people living in the same house are more similar than they are to the rest of the population).
The difficulty now is figuring out how we can shift this composition in later life. Unfortunately, downing a yoghurty probiotic drink containing a single strain of bacteria doesn’t really have much of an effect on the overall composition of the community in our guts. Many of the bacteria found in these drinks are not normally found in the guts of anyone – in fact they’re chosen largely because they can survive both the hostile journey from mouth to gut, and through the factory.
Our diets play a large role in the composition of our microbiome. And our microbiome populations become fixed during our early life. Differences in how we were delivered, whether we are breast fed or bottle fed, which country we grow up in and whether we share our house with pets, all affect the composition of our microbiome.
Perhaps the easiest way of shifting our microbiome is related to how much fibre we eat. Our bodies can’t digest dietary fibre on its own, and most of the fibre we eat makes its way to the end of our digestive tracts. This is where it feeds the bacteria in our guts, who in response not only increase their diversity (fibre feeds a lot of different kinds of bacterial species, who can all grow in its presence), but also release chemicals which are beneficial to our bodies’ health.
Poop pills: what do we know about this surprising possible obesity treatment?
However, there is another way we can shift our microbial population – faecal transplants. If we take an obese mouse, and feed its droppings to a lean mouse (thus transplanting its bacteria), that lean mouse will become obese – regardless of what it eats. The same is true if you take the gut bacteria from an obese human and transplant it into the gut of a lean mouse. That in itself is amazing.
But is the same true for humans? Well, faecal transplant (or FT) has been used clinically to treat C. difficile (or C-diff as it’s commonly known) infection. This nasty hospital-acquired infection is difficult to treat with standard antibiotics and, left unchecked, can be fatal. However, FT is an effective treatment for C-diff and is a cure for many people.
On the other hand, the literature surrounding its effectiveness for treating obesity in humans is controversial, and also risky. A lack of proper clinical trials means we don’t fully know whether it works or to what extent. Furthermore, FT has the potential to transmit a number of diseases, and given the increasing number of conditions that are being attributed to gut bacteria, the risk might just be too great given our level of understanding.
The bottom line: the future looks promising
So what’s the take home message? The microbiome is an exciting area of research, and undoubtedly will lead to treatments for a number of diseases in the future.
As it stands, our understanding is largely based on observational data – a case of correlation, rather than causation. But many people are confident causation is there, we just need the definitive proof.
In the meantime, the best thing we can do to feed our hungry bugs is to increase the amount of fibre in our diets and reduce unnecessary antibiotic use. The good news is that a lot of people are getting excited, and the gut microbiome is no longer the playground of just the microbiologists. Gut scientists, lung scientists and neuroscientists are all getting in on the action, and these collaborations are rapidly increasingly our knowledge of how the bacteria in our bowels are affecting our health. The time for the microbiome to really show its potential grows ever closer.