Play a Role in Obesity
Bacteria - Obesity, Weight Loss, Leptin - Bacteroidetes/Firmicutes
Not only do these microbes harvest from otherwise indigestible parts of our diet, but they also affect host biology so the nutrients can be stored," said Jeffrey Gordon, senior author on both Nature papers, and director of the Center for Genome Sciences at Washington University.
While each of us has a unique population of bacteria in our digestive tract, in general they fall into one of two bacterial divisions: the Bacteroidetes or the Firmicutes. And, which group is dominant may have an impact on weight.
Obese people and mice had more Firmicutes bacteria, while Bacteroidetes were the predominant bacteria in thinner individuals.
In one study, researchers harvested bacteria from the intestines of very fat mice with a gene defect that robs them of the hormone leptin. Leptin tells the brain to stop eating, and mice without it can get so fat that they can't even walk.
The researchers put this bacteria into a group of mice with no bacteria at all called germ-free mice. Without bacteria to help them digest their food, these mice are thinner than average. But, once these skinny mice are home to bacteria from obese mice, they bulk up.
A second group of germ-free mice given bacteria from normal-size mice also gained fat. But, the mice with bacteria from obese mice gained more, and they did it on the same diet as their thinner relatives.
"We looked at the total amount of body fat in the mouse before [the new bacteria were added] and after two weeks of being exposed. What we saw was mice given bacteria [from obese mice] had a 47 percent increase in body fat. The mice given bacteria from lean mice had a 27 percent increase in body fat," said Peter Turnbaugh, the lead author on the mouse paper.
In a second paper, researchers showed that diet affects gut/beneficial bacteria in humans. In this study, 12 obese people were put on either a reduced-fat or reduced carbohydrate diet.
With either diet, weight loss brought a shift in the dominant population of bacteria away from the efficient, fat-producing Firmicutes and toward Bacteroidetes. The shift occurred when a person on a low-fat diet lost 6 percent or more of body weight, or, when a person on a low-carbohydrate diet lost 2 percent or more of body weight.
It's too early to run to your doctor or the health food store looking for a way to alter your own gut/beneficial bacteria in hopes of a quick bacterial fix to fatness.
"We don't know the mechanism that controls the proportion of bacteria. We don't know how to shift the microbial ecology of gut," Mr. Gordon said.
"The question is, how to manipulate things without doing harm ... it's premature right now."
But beneficial bacteria may supply one piece of the puzzle in determining causes for the obesity epidemic in the United States.
In 1991, no state had an obesity rate of 20 percent, and only four had rates above 15 percent, according to the U.S. Centers for Disease Control and Prevention. Nine years later, 22 states had obesity rates of greater than 20 percent.
By 2005, only four states had obesity rates below 20 percent, and 17 states had rates greater than 25 percent, including three in which more than 30 percent of the population was considered obese.
Obesity rose dramatically in Ohio in the last 10 years. In 1996, 17.5 percent of Ohioans were obese. In 2005, and 24.5 percent were classified obese. In Michigan, 26.2 percent were obese.
"We really don't understand why rates of obesity are increasing," said Randy Seeley, an obesity researcher at the University of Cincinnati.
The Washington University research "opens up the possibility that one difference may have to do with our gut/beneficial flora/bacteria," he said.
That doesn't mean that greater availability of more calorie-dense food, our increasingly sedentary lives, or other things, such as lack of calcium in the diet, are not factors. But bacterial activity may be one more variable in a complicated picture.
Mr. Seeley, who wrote a commentary on the St. Louis research for Nature, said people should be cautious before blaming bacteria for all our travails on the scale.
"The ability of the gut flora to make a difference, even in these papers, is very small," he said.
Of course, weight gain is a matter of small effects, he said. It takes only an additional 11 calories per day -- "a potato chip" -- to add up to a pound in a year. The small effect of a single chip can, day after day, year after year, equal obesity.
So a small effect of gut/beneficial bacteria may have large consequences eventually.
"The second cautionary note is, we don't know what causes bacteria to become more of one type or the other," Mr. Seeley said. "It's relatively confusing. How could bacteria know whether they're in an obese person or a lean person, or that an obese person became a lean person? How do they know?" And why do they change.
In fact, Mr. Seeley notes, the fact that obese people have the more efficient bacteria "almost seems backward."
It seems logical that the body would try to extract more calories when weight is lower. In fact, many believe obesity is one consequence of our evolutionary need to survive food shortages.
But beneficial bacteria operates the other way.
"When you're starving to death, you would want the microbes to be more efficient," he said. "But that's exactly the opposite of what happens."
So we carry a mysterious, burgeoning population, capable of unknown things, within us. The 19th Century poet Walt Whitman never spoke truer words when he wrote, "I contain multitudes," although bacterial multitudes wasn't quite what he had in mind.
Because of these multitudes, our 46 chromosomes are just a fraction of the genome within us.
The bacterial genes we carry may be driven by the same evolutionary pressures changing bacteria in the external world.
"A lot of dramatic things have happened in way we live," Mr. Gordon said.
Our microbes may evolve "as our lifestyle changes, as our diets are altered, as our travel increases," he said. And, that may affect human biology.
Contact Jenni Laidman at: firstname.lastname@example.org or 419-724-6507.
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