We aren’t single individuals, but colonies of trillions. Our bodies, and our guts in particular, are home to vast swarms of bacteria and other microbes. This “microbiota” helps us to harvest energy from our food by breaking down the complex molecules that our own cells cannot cope with. They build vitamins that we cannot manufacture. They ‘talk to’ our immune system to ensure that it develops correctly, and they prevent invasions from other more harmful microbes. They’re our partners in life.
What happens when we kill them?
Farmers have been doing that experiment in animals for more than 50 years. By feeding low doses of antibiotics to healthy farm animals, they’ve found that they could fatten up their livestock by as much as 15 percent. You can put the antibiotics in their feed or in their water. You can give the drugs to cows, sheep, pigs or chickens. You can try penicillins, or tetracyclines, or many other classes of antibiotics. The effect is the same: more weight.
Consistent though this effect is, no one really understands why it works. The safe bet is that the drugs are exerting their influence by killing off some of the microbiota. Now, Ilseung Cho from the New York University School of Medicine has confirmed that hypothesis. By feeding antibiotics to young mice, he has shown that the drugs drastically change the microscopic communities within their guts, and increase the amount of calories they harvest from food. The result: they became fatter.
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.
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.
Many measures to curb the obesity epidemic are aimed at young children. It’s a sensible strategy – we know that overweight children have a good chance of becoming overweight adults. Family homes and schools have accordingly become critical arenas where the battle against the nation’s growing waistlines is fought. But there is another equally important environment that can severely affect a person’s chances of becoming overweight, but is more often overlooked – the womb.
Overweight parents tend to raise overweight children but over the last few years, studies have confirmed that this tendency to transcend generations isn’t just the product of a shared home environment. Obesity-related genes are involved too, but even they aren’t the whole story. Research has shown that a mother’s bodyweight in the period during and just before pregnancy has a large influence on the future weight of her children.
For example, children born to mothers who have gone through drastic weight-loss surgery (where most of the stomach and intestine are bypassed) are half as likely to be obese themselves. On the other hand, mothers who put on weight between two pregnancies are more likely to have an obese second child. In this way, the obesity epidemic has the potential to trickle down through the generations, like a snowball rolling its way into an avalanche.
Now, Robert Waterland from the Baylor College of Medicine has demonstrated how the snowball gains momentum by studying three generations of mice that have a genetic tendency to overeat. And using a special diet that was high in folate and other nutrients, he found that he could stop the snowball’s descent and spare future generations of mice from a heightened risk of obesity.
This is a quick follow-up to my other post on fat cells, which as it happens, isn’t the only obesity-related story out today. Another paper found a common genetic variant that increases the risk of obesity in its carriers.
A huge team of researchers scoured the genomes of almost 17,000 European people for genetic variations that are linked to obesity. Until now, only one has been found and it sits within a gene called FTO. This new study confirmed that FTO variants have the strongest association with obesity, but in the runner-up position is another variant near a gene called melanocortin-4 receptor or MC4R.
As fat people have an abundance of fat tissue, the natural assumption is that fat people have more fat cells, or ‘adipocytes‘. That’s only part of the story – it turns out that overweight and obese people not only have a surplus of fat cells, they have larger ones too.
The idea of these ‘fatter fat cells’ has been around since the 1970s. But their importance has been dramatically highlighted by a new study, which shows that the number of fat cells in both thin and obese people is more or less set during childhood and adolescence. During adulthood, about 8% of fat cells die every year only to be replaced by new ones. As a result, adults have a constant number of fat cells, even those who lose masses of weight. Instead, it’s changes in the volume of fat cells that causes body weight to rise and fall.
Kirsty Spalding from the Karolinska Institute in Sweden, together with a large team of international researchers, uncovered several lines of evidence to support these conclusions. Her study is a fascinating mix of cell counting, stomach surgery, radioactive Cold War fallout and a rather surprising use for carbon-dating.