...there is a difference in the bacterial taxonomic composition between obese and non-obese humans. They have shown that obese mice and people harbour in their guts a dominant population from the bacterial division Firmicutes. At the same time, lean people (or even those on a weight-loss diet) and lean mice, have less bacteria from the Firmicutes division and more from the Bacteroidetes division.
They found that in obese mice the gut bacterial population contained more enzymes that broke up complex carbohydrates, like starch. Other experiments showed that indeed, the population of bacteria in obese mice break up complex sugars more efficiently; that is, the bacterial populations of obese mice provide their hosts with smaller sugar molecules that are readily absorbed through the gut, creating a vicious feed-forward cycle: if you are a fat mouse, you will get more calories from the same piece of chow than if you are a lean mouse.
Their conclusion was that the human gut bacterial population is intimately connected with what we eat. High poly-carbohydrate foods eventually enrich their consumers’ guts with carbohydrate loving bacteria; and those, in turn, “reward” their hosts with the back-handed compliment of making more simple and easily absorbable carbohydrates available to them, making them fatter.
Consider a slice of whole wheat bread, about 100 calories.* This means that the actual caloric intake from a slice of bread will differ between individuals. Unfortunately, it is the fatter person who will, quite probably, receive more calories from eating the same slice of bread, because his gut bacteria will deliver more available calories to him.
Dhurandhar collected blood samples from 52 overweight patients. Ten of them, nearly 20 percent, showed antibody evidence of prior exposure to the SMAM-1 virus, which was a chicken virus not previously thought to have infected humans. Moreover, the once-infected patients weighed an average of 33 pounds more than those who were never infected and, most surprisingly, had lower cholesterol and triglyceride levels — the same paradoxical finding as in the chickens.
With Ad-36, Dhurandhar and Atkinson began by squirting the virus up the nostrils of a series of lab animals — chickens, rats, marmosets — and in every species the infected animals got fat.
“The marmosets were most dramatic,” Atkinson recalled. By seven months after infection, he said, 100 percent of them became obese.