Body weight could be down to more than simply what you eat - according to a new study, how you digest your food is also an important factor. Scientists have found that the bacteria in human guts, which help to break down food, differ in lean and obese people.
"Our findings suggest that obesity has a microbial component, which might have potential therapeutic implications," wrote the researchers, led by Jeffrey Gordon of Washington University in Missouri, in today's issue of Nature.
In the UK, more than a fifth of adults are obese and of the remaining population half of men and a third of women are classified as overweight. Worldwide, there are an estimated 300 million obese people and obesity is linked to heart disease, diabetes and premature death.
The amount of food a person eats relies on a complex interaction between hormones in the blood but Prof Gordon's work suggests the effects of the trillions of bacteria in the human digestive system - the microbiota, which help to break down otherwise indigestible foods - should also be taken into account.
The microbiota fall into two main categories: bacteroidetes and firmicutes. Prof Gordon's team found that obese people had a greater proportion of firmicutes to bacteroidetes than other people. When they followed 12 people who lost weight on low-calorie diets for a year, they found that the volunteers' proportion of bacteroidetes had increased. "They increased as the weight is lost and in proportion to the amount of weight loss," he said.
In an accompanying article in Nature, Randy Seeley of of the University of Cincinnati said Prof Gordon's research would play an important role in understanding the global obesity epidemic. "Although there is no doubt that human genetics plays a large part in determining body weight, it is equally undisputed that the increase in prevalence of obesity over the past 25 years cannot be attributed to changes in the human genome."
He suggested other factors that could be responsible, including cheap, high-calorie foods, a reduction in physical activity and now, with the publication of Prof Gordon's work, bacteria in our guts.
In an experiment on mice, Prof Gordon's team attempted to work out whether obese individuals started out with a particular proportion of bacteria that makes them prone to obesity, or whether the high proportion of firmicutes was a symptom of excess weight.
They transferred samples of the gut bacteria from obese and lean mice into two groups of microbiota-free mice. The mice given the "obese" bacteria extracted more calories from their food than those given the "lean" bacteria. They also found that the bacteria in obese mice was rich in genes for enzymes that broke down otherwise indigestible sugars. "The bacteria in obese mice seemed to assist their host in extracting extra calories from ingested food that could then be used as energy," Prof Seeley said. He said the results could change views of what caused obesity and how we depended on gut bacteria.
Prof Gordon said that if the results of the mice experiment were confirmed in humans, the bacterial profile of digestive systems could be used in future as a therapeutic target for treating obesity.
