Appetite is the healthy expression of the body’s need for fuel. When appetite goes wild, a craving is manifested. If the body really needs a particular nutrient urgently, the craving is legit, but if some trickster bugs hoodwink the body into believing it has to have a particular input right now, that’s a problem.
The various populations of bacteria that make up the gut microbiome generally work together well, but they do have their own agendas. Apparently, if Bug A isn’t happy about the incursions of Bug B, Bug A can convince its human host to commit chemical warfare by eating something that isn’t good for Bug B. While we prance around, kidding ourselves about free will, the “microscopic thugs” (so named by Billi Gordon, Ph.D.) are in charge.
The notion that they might run the show is gaining traction. This is from a 2013 study:
New studies show that bacteria, including commensal, probiotic, and pathogenic bacteria, in the gastrointestinal (GI) tract can activate neural pathways and central nervous system (CNS) signaling systems.
Three years later, evidence is piling up that tiny creatures can readjust our taste receptors, mess with our hormones, and tweak our reward systems. By regulating bile acids, they influence fat absorption. They affect the uptake of other nutrients too, and strengthen or weaken the integrity of the intestine’s lining. Lab work has shown that the microbiome regulates glucose and energy homeostasis. A lot happens down there.
After leaving the stomach, partly digested food travels approximately 20 feet through the three parts of the small intestine. Pancreatic enzymes and bile from the gallbladder flow into the duodenum. The jejunum is mainly about absorbing nutrients, and the ileum absorbs bile acids to be recycled. Throughout its length, “the small intestine activates sensing mechanisms that affect both glucose production and food intake.”
When food intake is affected, we’re back to talking about appetite and cravings, and obesity. Here is an interesting observation:
Duodenal nutrient sensing acts as a protective mechanism… [H]owever, this mechanism appears to be impaired after excess caloric intake.
Definitive demonstrations of the exact relationship between the microbiota and the intestine’s nutrient-sensing mechanisms have yet to appear, but it seems clear that a relationship exists. For instance, despite many remaining questions,
[…] recent advances in our understanding of the pathways regulating gut nutrient sensing provide compelling support for potential new therapeutic targets to restore glucose homeostasis in diabetes… [I]t is believed that the progression of obesity/diabetes can be attributed to the intestinal microbiota–host relationship.
It almost seems like too much to hope for — but what if millions of diabetics no longer had to stick themselves with needles? What if their lives could be normalized by reconfiguring their gut microbiota? That is a dream worth pursuing.
Meanwhile, it appears that the bugs can also influence enteroendocrine cells, and if they can, this is also worth knowing about.
Your responses and feedback are welcome!
Source: “Gut–brain axis: how the microbiome influences anxiety and depression,” Cell.com, 2013
Source: “Nutrient-Sensing Mechanisms in the Gut as Therapeutic Targets for Diabetes…,” DiabetesJournals.org, September 2013
Photo credit: Skley via VisualHunt/CC BY-ND
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