You are not alone. Even if you’re currently reading this in complete isolation, you are still far from a singular individual. You’re more of a colony – one human, together with microbes in their trillions. For every one of your own genes, your body is also host to thousands of bacterial ones. Some of the most important of these tenants – the microbiota – live in our gut. Their genes, collectively known as our microbiome, provide us with the ability to break down sources of food, like complex carbohydrates, that we would otherwise find completely indigestible.
Peter Turnbaugh from the Washington University School of Medicine has spent his career studying the microbiome. His latest work reveals both tremendous differences and similarities between the bacterial tenants of our digestive systems. Your bowels may be home to very different species of bacteria to mine, but both our sets share a core group of genes.
Turnbaugh likens the situation within our guts to that of islands. Real islands may be home to very different species of animals but all have representatives that perform certain roles; there will always be grazers, predators, insect-eating specialists, fishermen and so on. Across islands, animals approach a set of core lifestyles in different ways, and so it is with the microbiota – every man is an island, home to unique collections of bacteria that nonetheless carry out some core functions. And the further an person’s microbiota strays from this standard template, the more likely they are to be obese.
The discovery came about through a desire to see how similar the microbiota were between close relatives. Together with a large group of US scientists, Turnbaugh collected stool samples from 154 people to analyse their gut bacteria. The volunteers were broadly representative of the local population, had a range of different weights, and had not taken any antibiotics for at least half a year.
They included 54 pairs of twins, both identical and non-identical, and their mothers. Twins are a common feature of genetic studies – if a trait is strongly influenced by genes, you would expect identical twins, who share 100% of their genes, to be more similar in that trait than non-identical twins, who only share 50% of their genes. Indeed, identical twins have more closely matching BMI values than non-identical ones, and they gain weight after overeating in a more similar way.
Unsurprisingly, Turnbaugh found that the microbiotas of relatives are a closer match than those of unrelated people, even within similar weight categories. The reasons for this are unclear; it wasn’t because they shared a common environment, for twins who lived some distance away were no more dissimilar in their bacterial passengers than those who shared a home. Nor were the similarities driven by genes, for the microbiota of both identical and non-identical twins shared equally strong resemblances.
Relatives aside, individuals had extremely different gut bacteria, with few genetic similarities from person to person. No single species was present in more than 0.5% of the stool samples as a whole, and none were found in all the people involved. These differences between individuals were far greater than changes to any one person’s microbiota over time. Using a second set of samples, collected from the same people two months later, Turnbaugh showed that some bacterial groups had risen to dominance and others had fallen from power, but the players were largely the same.
At the genetic level, things looked quite different. The team took a more detailed look at the microbiomes of six of the families, three lean ones and three obese ones, and they found that the genes within all 18 microbiomes performed remarkably consistent jobs. They even had similar proportions of genes dedicated to different tasks. Although very high proportions were involved in breaking down carbohydrates and proteins, Turnbaugh found a relatively even spread of genes involved in various other ‘metabolic pathways’ – sequences of chemical reactions designed to break down potential nutrients.
The researchers also found membership of the microbiota depends on body weight. Compared to lean people, obese ones had fewer bacteria from the Bacteroidetes group and more from the Actinobacteria group. These results mirror earlier work by Turnbaugh’s group which showed that the Bacteroidetes were relatively rarer in obese mice than lean ones, and that their numbers rose in obese people who lost weight.
A closer look at the genes involved confirmed this analysis. Turnbaugh found about 383 genes that were activated to a greater extent in obese people than in lean ones and while the vast majority of these came from Actinobacteria species, none at all hailed from Bacteroidetes sources.
All in all, the obese twins had a less diverse milieu of gut bacteria than their leaner peers, which may be due to their comparative dearth of Bacteroidetes members. Turnbaugh compares the bowels of obese people to bodies of water that have been choked by agricultural run-offs. In such water, the bacterial community receives a substantial flood of nutrients, but its diversity plummets as a few species bloom and monopolise the extra energy. So it is with guts that have been flooded with calories.
Reference: Peter J. Turnbaugh, Micah Hamady, Tanya Yatsunenko, Brandi L. Cantarel, Alexis Duncan, Ruth E. Ley, Mitchell L. Sogin, William J. Jones, Bruce A. Roe, Jason P. Affourtit, Michael Egholm, Bernard Henrissat, Andrew C. Heath, Rob Knight, Jeffrey I. Gordon (2008). A core gut microbiome in obese and lean twins Nature DOI: 10.1038/nature07540
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