We left off with some of the questions that scientists were presented with in the course of learning more about the microbiome. Research showed that obese and lean people have different-size populations of various bacteria residing in their GI tracts, but right from the start it was also apparent that many other factors play a part.
For instance, the typical obese lab mouse has, overall, a paltry assortment of gut flora compared to the spectacularly diverse community that a lean mouse can boast of. Questions continued to arise. When the microbiome becomes altered, is it because of the inadequate diet? Or are the harmful changes indirect, caused by conditions created by obesity?
A team of Israeli scientists determined that microbes that thrive on artificial sweeteners are the same kind that other researchers had already found in excessive amounts, in the interiors of genetically obese mice. In recent years, many serious autoimmune conditions have been identified as emanating from chronic systemic inflammation, which originates in exactly one place, the gut.
Staphylococcus aureus and E. coli are both life forms that, for some reason, trigger human fat cells into producing inflammatory substances that irritate other cells and incidentally invite diabetes. Researchers have observed…
[…] a connection between certain types of bacteria and body fat that produces a heightened inflammatory response and drives the inflammatory process.
And then they found out about AD-36, the human adenovirus that apparently plays the dirty trick of changing adult stem cells into fat cells. More theories were proposed and more experiments designed.
At the University of Geneva, researchers kept mice very cold for as long as 10 days. Their inner bacterial universes adapted to the new reality. Some bug species prospered, while others failed to thrive.
When these hardy critters were transplanted into mice that had been intentionally engineered to have no microbiota of their own, the transplanted bugs helpfully facilitated the formation of more brown fat, and the recipient mice lost weight.
In the words of journalist Megan Thielking, the findings…
[…] suggested that harnessing the way cold changes the microbes in your body — and, consequently, the way you metabolize food — could be a potential avenue for fighting obesity.
Childhood Obesity News has mentioned Dr. Lara R. Dugas before. A physical activity epidemiologist, she has suggested redesigning the traditional school year because under the present system kids leave for the summer in relatively good shape and then slouch back to classes in the fall all bloated and misshapen.
The worst victims of this phenomenon are girls in the low-income and minority demographics. The NIH.gov website says of a study where Dr. Dugas was lead author:
A newly identified factor, the gut microbiota, which is a bacterial ecosystem residing within the gastrointestinal tract of humans, has now been implicated in the obesity epidemic. Importantly, this bacterial community is impacted by external environmental factors through a variety of undefined mechanisms.
In other words, just a year ago, the existence of our three or four pounds of bugs, constituting a separate and discrete organ, was still being referred to as a “newly identified factor.” And today, the microbiome’s mechanisms are not much better defined or understood than they were last July.
Your responses and feedback are welcome!
Source: “Regulation of Appetite, Satiation, and Body Weight by Enteroendocrine Cells,” Karger.com, February 2015
Source: “Artificial Sweeteners May Change Our Gut Bacteria in Dangerous Ways,” ScientificAmerican.com, 03/17/15
Source: “Chronic Inflammation: How Majority Of Inflammatory Diseases Start In Your Gut,” Reset.me, 11/21/15
Source: “The Truth about Freezing your Fat Off,” TheWeek.com, 01/08/16
Source: “The obese gut microbiome across the epidemiologic transition,” NIH.gov, 01/11/16
Photo credit: Global Panorama via Visualhunt/CC BY-SA
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