Every time you have a meal, you’re eating not just for yourself, but for the hundred trillion bacteria that line your large intestine. This live-in colony of microbes, which together can weigh several pounds and consists of hundreds of individual species, is a digestion powerhouse, breaking food down into useful and nutritious components for us and for the microbes. It’s only recently that new genomic techniques have opened the doors to detailed study of our gut microbiome, but understanding how it varies among different people is extremely important. Scientists suspect that the make-up of the inhabitants of our guts might help explain why some people develop metabolic disorders and others do not, and why some people put on weight while others stay thin.
But assessing cause and effect when it comes to the microbiome is difficult. When a person or a mouse with a particular set of bacteria is obese, is the obesity influencing the gut flora or are the gut flora contributing to the obesity? Can we change the makeup of our gut bacteria by changing the way we eat? While researchers have probed some of these questions using mouse models, and have come up with some fascinating answers—for instance, you can make a mouse obese by giving it gut microbes from an obese mouse, suggesting that at least in mice, gut flora do influence obesity—studies in humans are required for answers that could be applicable to real life. A pair of studies out this week in Nature, from two European consortia devoted to the study of the gut microbiome, add new insights into this question.
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One study, organized through the pan-European MetaHIT consortium, examined the bacterial genes present in the stool of nearly 300 Danish volunteers, both lean and obese, as well as markers of metabolic health. That team found that having a relatively low genetic diversity in one’s microbiome correlated with higher inflammation, greater insulin resistance and other warning signs of metabolic diseases. Obese participants who had low diversity also gained significantly more weight over the course of nine years, the team reported.
The other study, from the ANR MicroObes consortium of researchers in France, put 49 French volunteers, all overweight or obese, on a low-calorie diet. Strikingly, the participants who had low genetic diversity in their microbiomes at the beginning saw their diversity increase and their metabolic markers improve on the diet. People who already had high diversity didn’t see nearly so much improvement, suggesting that perhaps a low-diversity microbiome, though linked to worse metabolic health, is amenable to dietary intervention.
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Having low diversity does not mean that someone is necessarily obese or overweight. Of the 292 Danes in the first study, 169, or 57%, were obese, but only 23% of the whole group had low genetic diversity. There were obese people in both studies who had high genetic diversity. Rather, low diversity may be a risk factor for developing a metabolic disorder of the sort that often, but not always, accompanies obesity, like type 2 diabetes, says Dusko Ehrlich of the French National Institute of Agronomic Research, an author on both papers.
It’s tempting to consider the kind of strategies this new classification might provide in the fight against obesity and metabolic diseases. It suggests the possibility of identifying via the microbiome people who, though obese, may be relatively healthy, and alerting those who may not yet be obese or suffer a metabolic illness that they may be at higher risk of both. At this point, however, the next stage is to continue studying these and other groupings of gut microbiomes, and to explore the nature of the relationship between specific bacteria and metabolism, wrote two scientists who were not involved in the work, Sungsoon Fang and Ronald M. Evans of the Salk Institute, in a commentary piece in the same issue of Nature.
Research on the gut microbiome is still so new, and the bugs within us so little known, that many of the bacteria uncovered by studies like this one are still without names, descriptions or sequenced genomes. Fully 90% of the bacterial genes uncovered in the Danish study could not even be assigned to a specific bacterial genome. There’s a rainforest in our guts, and we’re just beginning to explore it.
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