Clues to an Elusive Ghrelin-Microbiome Tie

Incredibly, there are still more dots to connect in the microbiome story, because the colonies of bacteria that live inside us seem to stick their meddling fingers into every aspect of our lives. Yesterday, we talked about the cravings dot. Granted, a craving can be positive, like when a person craves a tuna sandwich because the body needs a dose of protein. But unfortunately, cravings are often for things we really shouldn’t eat at all, ranging from doughnuts to burnt matches, and usually lead to grief.

Then, there is appetite, which is similar to craving but not the same. Appetite is generally considered a desirable thing to possess. If an endogenous chemical did not remind us to eat, we might forget and starve. Appetite is what people lose when taking certain medications and undergoing certain treatments, and medical science strives to restore appetite to them because a sick person needs good nutrition.

We know that upset feelings often result in the urge to comfort-eat, or binge-eat. An important question is whether bacteria are involved in that transaction. Apparently the bugs that compose the microbiome can influence the happiness hormones.

Presumably, corralling the bugs into good order could change a person’s emotional landscape enough that they no longer eat to “stuff their feelings” down. What else might the microbiota do?

Weird ghrelin

Childhood Obesity News has spoken before of ghrelin, the “hunger hormone.” It originates mainly in the stomach and small intestine (where most of our native bacteria hang out) and in several other bodily locations as well. The substance is produced by “specialized cells,” and it would be interesting to know whether anyone suspects that those cells might be not our own. It’s not impossible that this chemical comes from one of the many species of bacteria that inhabit us.

Some people are positive they know what ghrelin is all about, and that it increases when the body is in negative energy balance and decreases when the energy balance is positive. Others wish that it could be so simple. There is little certainty about this substance, except that it appears to be reduced when the body is overwhelmed by too many H. pylori, an organism that is, like ghrelin, little understood and much reviled. Paradoxically, an overgrowth of candida albicans appears to increase ghrelin, and so does the chronic digestive tract inflammation called celiac disease.

An overabundance of ghrelin flips the switch from “eating to live” to “living to eat,” but that is not the reason why a previous post labeled it as weird. (Look for the sentence that reads, “Then, they measured the levels of ghrelin in the participants’ bodies — which reacted exactly as if those pretend calorie counts had been real.”)

In other words, psychosomatic ghrelin fabrication. Also, any interested party may follow up on a report titled “Ghrelin fluctuation, what determines its production?,” which contains this fascinating tidbit:

The pre-prandial surge of ghrelin may be induced largely by the expectation of food. The signal is discharged from the central nervous system and transmitted to stomach through the efferent fiber of vagus nerve…

As with Pavlov’s salivating dogs, the body can apparently be induced to generate ghrelin through mind power alone. The same journal article also says:

However, the current understanding about the regulation of ghrelin level, especially its mechanism, is far from satisfaction, with much discrepancy among studies. Unanimous conclusion on some critical topics is still lacking, reflecting the remarkable complexity in the regulation system…

In addition, many previous reports identify only correlation between ghrelin and a certain agent, but cannot distinguish whether the change in ghrelin level is the cause or effect, or they are actually independent. Thus, future works need to discover agents that have more direct and significant effect on ghrelin secretion, confirm the causality, and elucidate the underlying mechanism of its regulation.

That last part, about how science needs to discover “agents that have more direct and significant effect on ghrelin secretion,” and the parts about causality and the underlying mechanism of its regulation, leave open the possibility that the intestinal bacteria are up to something. Here is a sentence that might be very significant in this regard:

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.

Is that sinking in? The critters that live in our intestines, amongst all the ghrelin and other interesting chemicals, also have the ability to “activate neural pathways and central nervous system signaling systems.”

Ghrelin is only a small part of the mystery. Science at the moment quite frankly does not know what is going on. Science is like the baffled husband in an old-time detective movie, pretty sure his wife is stepping out. But when, and where, and why, and how long has this been going on? And who is the low-down son of a gun, anyway?

Your responses and feedback are welcome!

Source: “Ghrelin fluctuation, what determines its production?,”, 2009
Source: “Gut–brain axis: how the microbiome influences anxiety and depression,”, 2013
Image by: Jessy Rone

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About Dr. Robert A. Pretlow

Dr. Robert A. Pretlow is a pediatrician and childhood obesity specialist. He has been researching and spreading awareness on the childhood obesity epidemic in the US for more than a decade.
You can contact Dr. Pretlow at:


Dr. Pretlow’s invited presentation at the American Society of Animal Science 2020 Conference
What’s Causing Obesity in Companion Animals and What Can We Do About It

Dr. Pretlow’s invited presentation at the World Obesity Federation 2019 Conference:
Food/Eating Addiction and the Displacement Mechanism

Dr. Pretlow’s Multi-Center Clinical Trial Kick-off Speech 2018:
Obesity: Tackling the Root Cause

Dr. Pretlow’s 2017 Workshop on
Treatment of Obesity Using the Addiction Model

Dr. Pretlow’s invited presentation for
TEC and UNC 2016

Dr. Pretlow’s invited presentation at the 2015 Obesity Summit in London, UK.

Dr. Pretlow’s invited keynote at the 2014 European Childhood Obesity Group Congress in Salzburg, Austria.

Dr. Pretlow’s presentation at the 2013 European Congress on Obesity in Liverpool, UK.

Dr. Pretlow’s presentation at the 2011 International Conference on Childhood Obesity in Lisbon, Portugal.

Dr. Pretlow’s presentation at the 2010 Uniting Against Childhood Obesity Conference in Houston, TX.

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