Obesity linked to intestinal bacteria

Blame fat on the bacteria - again

By Thomas H. Maugh II

Los Angeles Times Staff Writer

January 6, 2007

Bacteria in the intestines can modify the body's chemistry to alter the amount of food that becomes stored as fat, according to a finding in mice reported this week that could help in controlling obesity.

A team [Geoffrey Gordon and Ruth Ley] from the Washington University School of Medicine in St. Louis had reported last month that obese mice — and humans — have an unusually high proportion of a family of intestinal bacteria that are exceptionally efficient at breaking down complex sugars in the diet into a form that is readily absorbed. The upshot is that the bacteria make more calories available to the body from a given quantity of food, leading to weight gain.

The same group reported in the current Proceedings of the National Academy of Sciences that the bacteria also play a more direct role, manipulating body chemistry to increase the amount of food stored as fat...

The bacteria suppressed production of a hormone called fasting-induced adipose factor,

The bacteria also suppressed production of another enzyme, called adenosine monophosphate-activated protein kinase, which is used by the body to burn stored fat for energy. Lower levels of the enzyme make weight loss more difficult.

The net effect is that the bacteria not only make more calories available to the body, they encourage the body to store that energy as fat and keep the fat on.

One interesting "systems" feature of this result is that it may reveal another pathway, off the normal maps, for psychosocial factors, particulary social stress, to use to influence obesity - which we know happens.

It was only relatively recently realized that another bacteria (H. pylori) was heavily involved in human development of peptic ulcers.

Both of these may be cases where our "biomedical model" of the boundaries of a human being's physiology turn out to be too restrictive, and we need to expand the boundaries outwards to include topologically external factors and even other species as having a directly linked ecological effect on "human" digestion.

That, in turn, supports the mental model I've suggested, that any factor, regardless how distal, that can get itself into a phase-lock loop with human physiology has to be, mathematically, considered as "real" and as "part" of human physiology as organs such as the liver. In a very real regulatory feedback loop control sense, the closer we look, the less it appears that "we" are separate individuals walking around with big gaps between us, and between us and "other species."

The implications are that to study epidemiology or to design health interventions, we need to be guided by a map of regulatory feedback control space, not just a map of the physcial world our unassisted eyes report to us. That makes impacts on "personal health" that are "caused" by changes in social interaction, now well documented, to be less mysterious and more "obvious."

Link to NPR audio coverage of same story and many related stories on the epidemic of obesity.

CNN Coverage.

CDC - Centers for Disease Control and Prevention - on Overweight and Obesity in general.

(Photo credit - jege which I selected because I thought the key point here was the psychological resistance to meeting a new species and realizing we need to include it in our lives.)

technorati tags:Ley, Gordon, Obesity, microbial, ecology, bacteria, systems, overweight