Where Cravings Are Bred
The trillions of microbes in your gut have ways of enforcing their own nutrient needs.
By Hara Estroff Marano published March 7, 2023 - last reviewed on March 7, 2023
Ask not how your diet affects your gut microbiome but how the microbiome affects your diet. A ripening harvest of studies suggests that the microbes in your gut not only manage your appetite but manipulate your food choices. It’s their way of ensuring that their own needs are met.
Hunger is a highly fortified drive, fed through many biological pathways coordinated by the hypothalamus. After all, the most basic requirement for existence is getting enough energy and nutrients to power life.
Hormones produced in the brain generate feelings of hunger and stimulate food intake, while others originating in the gut urge us to eat. A rich stew of yet other hormones —some produced in the brain, some produced by fat tissue (where extra energy is stored), but most generated by the gut and affiliated organs—stimulate feelings of satiety and inhibit feeding. The variety of signaling mechanisms assures that hunger is expressed in multiple types of discomfort—a rumbling stomach, irritable mood, light-headedness—all goading you to get some food, definitely a survival advantage before there was a pizza place on every corner.
Then, of course, there are the many inducements to eating (or not) that go beyond physiologic hunger and influence appetite. The sight of that bubbling pepperoni pizza. The smell of fresh-baked bread. The stress of an important deadline. Boredom.
To the already full pot of signals directing what you put in your mouth and when, add one more—the everyday activity of the trillions of bacteria inhabiting your intestinal tract, collectively known as the gut microbiome. Their genes outnumber ours 100 to 1, giving them the might to shift our eating behavior in ways that benefit them. Germ-free mice colonized by the microbiome of wild rodents with distinctly different natural feeding strategies—some herbivores, some not—adopt the eating patterns of the donor rodent.
Through their direct actions, through their metabolic products, through messages whisked up the vagus nerve from gut to brain, and even via their Darwinian competition for dominance, gut microbes directly and indirectly engineer what you eat and, it is thought, especially dictate your cravings: a protein-rich chicken breast or a bacon-clad cheeseburger?
Gut bacteria can create cravings by playing with your taste receptors, altering the ability to sense and taste nutrients. For example, they can decrease sensitivity to sweet and fatty tastes, driving the need for greater intensity of such stimuli. A gut well-populated by Lactobacilli, important in keeping pathogenic bacteria in check, decreases sensitivity to sour taste. Gut bugs can also increase sensitivity to bitterness—explaining, perhaps, why you can’t countenance broccoli.
Working through chemosensory signaling pathways, the components of various bacteria, or their metabolic byproducts, alter expression of taste receptor cells both in the intestines and in the mouth, although the full menu of ways they do it is not yet written. Nevertheless, shifts in the gut microbial ecosystem can steer food choice by significantly affecting taste perception—the most important driver of food consumption.
Gut bacteria can also influence food choice by commandeering neurochemical circuits in the hypothalamus. Microbes produce proteins that share molecular sequences with various hunger and satiety hormones and can masquerade as such hormones, interfering with normal appetite regulation. They can, for example, bind with receptors for hormones and prolong their activation or, as antagonists, block it. Researchers have found that gut
microbes can reduce the brain’s sensitivity to leptin, a major hunger-suppressing hormone released by body fat.
Masquerade is not their only game. Various microbial components and metabolites also openly act as appetite-related signaling molecules. As they live, feed, and die, bacteria discharge cell components (for example, lipopolysaccharides) that activate production of the satiety hormone cholecystokinin (CCK), which is manufactured and released by cells lining the small intestine. CCK inhibits food intake both by interacting with leptin and by directly circulating to the brain and triggering the hypothalamus to curtail appetite.
Defense by Diversity
Short-chain fatty acids (SCFAs) are a whole other avenue of influence. Biologically active substances produced in the lower intestines by the action of various species of gut bacteria (Bifidobacteria, Lactobacilli, Roseburia) on fiber-rich foods otherwise resistant to digestion, SCFAs have many important functions.
They maintain the integrity of the gut wall. They regulate the acidity of the gut, preventing overgrowth of infectious species. They boost immunity. They foster mental health by stimulating neuroplasticity in the brain. They also play a big role in appetite control. The SCFA acetate, for example, inhibits specific neurochemicals in the hypothalamus that otherwise increase appetite and decrease metabolism. Its sibling SCFA butyrate is something of an appetite-regulating superstar: It affects the metabolism of fats in multiple ways that suppress feeding and influences the action of several hunger-related hormones.
The species of Roseburia that produce butyrate, along with the bacteria that generate the other SCFAs, can’t do their important work unless they have fiber-rich foods to feast on. Yet the trillions of other gut bacteria have their favorite foods, too. Yeasts demand sugar; Prevotella prefers starchy carbohydrates. And they all clamor and compete to be fed. The absence of key nutrients shifts the balance of microbes in the gut, with the surviving species disproportionately demanding to be fed.
As if SCFAs don’t have a large enough portfolio of assignments, they also promote microbial diversity, primarily by nourishing many other bacteria. Maintaining microbial diversity turns out to be the best way to keep appetite under control. Diminished diversity is inherently marked by increased prevalence of some species over others; the constrained competition makes it easier for them to enforce their meal preferences.
Generally, a decline in diversity of gut microbes is associated with hunger, whereas a full battalion of bugs is linked to satiety. In just one example, animal studies indicate that gut microbial richness promotes leptin signaling of satiety and prevents overeating. Bariatric surgery, also known as gastric bypass, done to help the morbidly obese lose weight, is now believed to work not because it limits the amount of food people consume but because it changes the composition of the microbiome in an enriched direction.
On the Menu
Gastric bypass surgery is an extreme means of establishing a healthy microbiome. There are, of course, noninvasive ways to do so. The most straightforward is to eat a diverse diet especially rich in fruit and vegetables, foods that nourish many beneficial bacteria. Another is by consuming supplements of fiber-rich prebiotics and bug-bundled probiotics. The ways are not mutually exclusive.