It Takes Guts
It Takes “Guts” to Stop Eating:
New obesity research shows overeating may be the fault of microbes in the gut.
If the lengthy national conversation about our obesity epidemic doesn’t take weight off your shoulders, you’re not alone. The truth is, our country’s myriad diets and articles on pinching pounds aren’t clearing any weight off our bellies, hips, or anywhere else.
Those looking to lose weight with these programs keep reverting to their baseline because of bacteria in the gut that can govern our cravings.
Despite these concerns, there has been very little data about the exact mechanisms that separate those who eat until feeling full and maintain a healthy weight and those who consume much more food and have a consequent weight problem. Frequently, we simply say that one person has a more ‘active’ metabolism than the other.
However, new research reveals an extensive metabolic interplay that has been previously obscured. It seems that we have ubiquitous companions undermining our self-control and sending us unwanted signals. And I don’t mean friends or relatives. I’m talking about the trillions of microbes that live inside the gut and perform essential bodily functions. 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 gut bacteria play a critical role in obesity. It is now understood that certain strains of bacteria are associated with an increase in the consequences of obesity such as insulin resistance, type 2 diabetes, hypertension, and elevated blood lipids. Until now, our working model for appetite and satiety was based upon the assumption that this aspect of obesity was dependent upon an intrinsic gut-brain axis of circulating gut-tissue molecules and hormones and was unrelated to the microbiome.
Our assumption was 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
Recent research has uncovered that gut bacteria play a critical role in obesity. It is now understood that certain strains of bacteria are associated with an increase in the consequences of obesity such as insulin resistance, type 2 diabetes, hypertension, and elevated blood lipids. 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 directly participate in the body’s triggering mechanisms determining both hunger and fullness.
There is an immense amount of microbial life 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, known 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 were only given small amounts of food. Upon administration of this specific bacterial protein, the unfed rodents either significantly diminished their food intake or stopped eating completely. This experiment demonstrated that the bacterial proteins from E. coli are involved in the same pathways of hormonal stimulation used by our own cells to issue signals to the brain indicating sensations of hunger and fullness. Based on this research, it is estimated that it takes an increase of about 1 billion extra bacteria in the stomach before the growth phase switches from active growth to the more static phase associated with the production of proteins linked to satiety.
Additional research should clarify further aspects of this dynamic and hopefully lead to better treatments for obesity in the future. It is becoming clear that any pathway toward real success will be based upon a deeper understanding of how the microbiome interacts 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 going to be my excuse.
William B. Miller, Jr., MD has been a physician in academic and private practice for more than 30 years. He is the author of The Microcosm Within: Evolution and Extinction in the Hologenome. // themicrocosmwithin.com