There is a widespread belief, that being overweight or obese is a question of failing willpower, fuelled in no small part by food, fitness and beauty industries. But if we look at the issue of obesity through a scientific spyglass, a very different picture emerges. Genes, for example, exert a large influence on our tendency to become obese often by influencing behaviour – a case of nature via nurture. But it’s not just our own genes that are important.
In terms of processing food, humans are hardly self-sufficient. Our guts are the home of trillions of bacteria that help to break down foodstuffs that our own cells cannot cope with. Together the genes expressed by these intestinal comrades outnumber our own by thousands of times, and yet we are still largely in the dark what they do.
Over 90% of these bacteria, collectively known as the microbiota, come from just two groups – the Bacteroidetes and the Firmicutes. Now, new research suggests that the proportion of these groups is linked to the risk of becoming obese.
Ruth Ley, Peter Turnbaugh, Jeffrey Gordon and colleagues at Washington University first noticed the link between the microbiota and obesity by studying a special strain of fat mice. These mice lack the hormone leptin, which controls the body’s ‘fat thermostat’. Without it, the mice cannot monitor the amount of fat in their body and quickly become obese through overeating.
The team noticed that these mice had 50% fewer Bacteroidetes and 50% more Firmicutes in their bowels than their lean counterparts. They saw the same thing in humans. The relative proportion of Bacteroidetes increased in obese people as they lost weight through low-fat or low-carbohydrate diets, while the Firmicutes became less abundant.
The link between the microbiota and obesity became even clearer when Gordon looked at a special strain of mice with no microbiota of their own. These intestinal tabula rasas proved to be strongly resistant to the fattening effects of unhealthy diets. After eight weeks on a 40% fat diet, these animals put on less than half as much weight as their normal peers, despite eating the same amount of food. When the team transplanted the microbiota from fat and lean mice into the germ-free strains, those colonised by microbiota from fat donors packed on far more weight than those paired with lean donors.
To find out why the shifting bacterial balances were affecting body weight, Gordon and co. compared the microbiota of fat and lean mice at a genetic level. Samples from fat mice showed much stronger activation of genes that coded for carbohydrate-destroying enzymes, which break down otherwise indigestible starches and sugars. As a result, these mice were extracting more energy from their food than their lean cousins.
The bacteria were also manipulating the animals’ own genes, triggering biochemical pathways that store fats in the liver and muscles, rather than metabolising them. While these effects are relatively small, Gordon believes that they can lead to very large fluctuations in weight, over the course of months or years.
Obviously, the microbiota are not the whole story behind the obesity epidemic. We now need to understand how they interact with other things that affect our risk of becoming obese, not least of all, our own genes. And there is much we still don’t know about our life-long passengers, such as how they sense and respond to their host’s condition, how they are passed on, or how they are affected by our diet. By answering these questions, scientists could then assess whether actively shifting our bacterial balances could help to stem the worldwide increase in obesity levels.
Reference: Ruth E. Ley, Peter J. Turnbaugh, Samuel Klein, Jeffrey I. Gordon (2006). Microbial ecology: Human gut microbes associated with obesity Nature, 444 (7122), 1022-1023 DOI: 10.1038/4441022a
Peter J. Turnbaugh, Ruth E. Ley, Michael A. Mahowald, Vincent Magrini, Elaine R. Mardis, Jeffrey I. Gordon (2006). An obesity-associated gut microbiome with increased capacity for energy harvest Nature, 444 (7122), 1027-131 DOI: 10.1038/nature05414
An introduction to the microbiome
October 6th, 2008 at 1:10 pm
“These intestinal tabula rasas proved to be strongly resistant to the fattening effects of unhealthy diets. After eight weeks on a 40% fat diet, these animals put on less than half as much weight as their normal peers, despite eating the same amount of food.”
I’m sorry if this is a dumb question, but…could this be largely because these mice don’t have the bacteria in their guts to help them absorb nutrients/calories from food? I mean, correct me if I’m wrong, but humans who have diseases that interfere with gut absorption (e.g., celiac sprue) tend to stay pretty thin, even when they eat a lot, just because they’re not absorbing the nutrients from the food they eat.
I don’t doubt the results of the study. I’m just wondering how comparing mice with no biota (and therefore–I assume–a diminished capacity for calorie absorption) to mice with biota is relevant to an investigation of how the ratio of one group of microcritters to another affects body weight. Seems kind of like comparing apples to oranges.
(Really, I am curious. I’m not any kind of life science/nutrition/statistics person at all, but I’m always curious about experimental design.)
October 6th, 2008 at 2:59 pm
I think the biota-free mice are required to show that the biota composition differences do cause some weight difference, rather than just reflecting one.
It’s known that gaining or losing weight changes the composition of the microbiota, but microbiota-free mice can easily be manipulated to see if changing the biota composition can cause weight gain or loss.
October 6th, 2008 at 3:23 pm
Are these the same two groups of microbiota whose relative population is altered by Echinacea?
October 7th, 2008 at 5:59 am
Okay, I understand that biota-free mice can be inoculated with biota in different ratios to see how that affects weight loss/gain, and that makes sense. But the review implies that the fact that the biota-free mice, while still biota-free, did not gain weight is significant.
I’m also curious about overall health. Are biota-free mice healthier/longer-lived than their bacteria-ridden cousins? Are the mice with higher ratios of Bacteroidetes to Firmicutes less healthy, or just fatter?
October 14th, 2008 at 3:02 am
A key phrase:
This seems to be the main no evidence of causality from microbiota to fatness. On the other hand, the change in the nature of the microbiota when people lost weight suggests causality in the other direction – fatness/excessive food intake changing the microbiota.
June 22nd, 2009 at 2:49 am
I don’t see how this shows obesity is not a failing of willpower in any way, sorry. Even given that the study is entirely correct and assuming that the populations of gut bacteria are not driven in any way by people becoming obese through failures of will, all this means is that obese people will absorb a few more calories from food than lean people. This does not mean that they cannot restrict food intake and increase energy expenditure to lose weight. It means that it may, or may not, be a little harder. This finding may not even affect the subjective difficulty of calorie restriction in any way! To say that findings like these somehow disprove the notion that body composition is under conscious control is wholly unscientific.
March 4th, 2010 at 11:48 am
it’s not a question of will power, but the simple fact, that masses of bacteria are linked and send chemical messengers to each other – case in point – the plaque in your mouth is a bio-film and the bacteria communicate when they reach critical mass and form the film itself. these gut bacteria send out “Feed me carbs or feed me fat” messages to you, the host, to ensure their survival. if you don’t comply, they start to die off and you feel awful from the exotoxins in their cell walls. eating the offending foods stops the discomfort, so you become essentiually addicted.
if you want to test this out, stop eating gluten and dairy for 2 weeks. if you feel worse at first, i am right!
March 4th, 2010 at 12:38 pm
it’s not a question of will power, but the simple fact, that masses of bacteria are linked and send chemical messengers to each other – case in point – the plaque in your mouth is a bio-film and the bacteria communicate when they reach critical mass and form the film itself. these gut bacteria send out “Feed me carbs or feed me fat” messages to you, the host, to ensure their survival. if you don’t comply, they start to die off and you feel awful from the exotoxins in their cell walls. eating the offending foods stops the discomfort, so you become essentiually addicted.
if you want to test this out, stop eating gluten and dairy for 2 weeks. if you feel worse at first, i am right!