It takes ‘guts’ to stop eating: Obesity and the Microbiome


miller-wideFor many years, there has been an extensive national conversation about our epidemic of obesity and it’s health consequences. Endless articles have been written and myriad diets are touted. Yet, most dieters don’t lose any significant weight on any regimen, and for those few who do, it is often only a temporary weight loss with most people reverting back to their original baseline after a few months. The causes for the persistence of this latter phenomenon have never been clearly understood, but the most frequent explanation is that the overweight individual simply lacks self-control.
Despite all these concerns, there has been very little data about the exact mechanisms that separate someone who eats till feeling full and still maintains a normal weight compared to another individual who also eats till full, but has consumed much more food and has a consequent weight problem. Frequently, we simply say that one person has a more “active” metabolism than another.
However, new research is revealing an extensive metabolic interplay that has been obscured until very recently. It seems that we have ubiquitous companions undermining our self-control and sending us unwanted signals. And I don’t mean your friends or relatives. I’m talking about the trillions of microbes that live inside our gut and perform essential services to us.

Previous research reports have revealed that the gut microbiome has a startling range of influences. These microorganisms serve a crucial role in mediating our immune systems, metabolism and central nervous system, assisting in normal growth and development, and protecting us against unwanted pathogens. Our gut microbes even affect our mental state and have been linked to depression and anxiety.
In addition, recent research has uncovered that our gut bacteria play a critical role in obesity. Furthermore, it is also now understood that certain strains of bacteria are associated with an increase in the consequences of obesity, such as insulin resistance, Type II diabetes, hypertension and elevated blood lipids. Until now, our working model for appetite or satiety was based upon the assumption that this aspect of obesity was dependent upon an intrinsic gut-brain axis of circulating molecules and hormones and was not unrelated to the microbiome.
Our assumption had been that when people eat and begin to digest, gut tissues send signals of fullness and satisfaction to specific centers in the brain, such as the hypothalamus or amygdala in which the nutritional and sensory aspects of food trigger an eating control regulatory circuit. However, recent research has just demonstrated that our gut microbes are directly participating in that circuit by giving off bioactive molecules that tell us whether we are full or still hungry, and surprisingly, this circuit is dependent on their assessment of their own needs. The other circuits certainly exist, but gut bacteria can produce some of the same types of chemicals that regulate satiety, such as proteins and peptide hormones that are part of the regulatory system of our own cells. So our gut bacteria are directly participating in the body’s triggering mechanisms determining both hunger and satiety.

An immense amount of microbial life exists in the stomach and intestine. A new study from researchers in France investigated proteins that are produced by one type of bacteria in the stomach, know as E. coli. When we eat, these bacteria go through a biphasic pattern of response to the nutrients entering our stomach. At first, they begin to multiply very rapidly, producing one set of proteins. After about 20 minutes of eating, the bacteria stop their rapid growth phase and begin to produce other proteins that are distinct from the earlier products of bacterial metabolism produced during the most active period of their reproductive cycle. It is the second type of protein that seems to directly influence our feelings of satiety.

To prove the connection, the researchers injected this second type of protein into rodents that had not been fed or only given small amounts of food. Upon administration of this specific bacterial protein, these hungry rodents either significantly diminished their food intake or stopped eating completely. This experiment demonstrated that the bacterial proteins from the E. coli are involved in the same pathways of hormonal stimulation used by our own cells to issue signals to the brain indicating hunger or a sensation of satiety. Based on this research, it is estimated that it takes an increase of about one billion extra bacteria in the stomach before the growth phase switches from active growth to the more static one associated with the production of proteins linked to satiety. So although it may take a village to raise a child, it takes about 1 billion more bacteria to make each one feel full.
Additional research should clarify further aspects of this dynamic and hopefully lead towards better treatments for obesity in the future. It is becoming clear that any pathway towards real success will be based upon a deeper understanding how our crucial microbiome as our obligatory companions interact with our intrinsic regulatory mechanisms.

As for my own gut microbes, I’m pretty certain that they prefer chocolate chip cookies. For now, that’s definitely going to be my new excuse.

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Dr. William B. Miller Jr.
Dr. William B. Miller, Jr., has been a physician in academic and private practice for over 30 years. He is the author of The Microcosm Within: Evolution and Extinction in the Hologenome. He currently serves as a scientific advisor to Prebiotin. For more information, visit


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