Food Cravings: Your Gut Microbes Might Be to Blame

Shin

Subtitle: 5 arguments that gut microbes can manipulate food choices.

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Resisting food cravings can be a nightmare for some and a struggle for many. While the cause of food cravings itself is multifaceted — encompassing environmental, cultural, social, psychological, genetic, and behavioral (habits) factors — scientists have pondered on the microbial aspects as well.

Given that the gut-brain axis is well established in modern biology, it’s quite imaginable for gut microbes to induce cravings in the brain. As Professor Carlo Maley, director of the Arizona Cancer and Evolution Center and the first president of the International Society for Evolution, Ecology, and Cancer, wrote as a senior co-author in BioAssays: “Gut microbes may manipulate host eating behavior in ways that promote their fitness at the expense of host fitness.”

This idea first stems from a classic example that a microbe can directly manipulate host behavior. The parasite Toxoplasma gondii enters the rodent’s brain, making it lost its sense of fear for cat’s urine. Instead, infected rodents became attracted to cat’s urine — “a propensity that promotes the transmission of T. gondii at the expense of the fitness of the rat,” they said.

The same may apply to food cravings — that those gut microbes somehow convince the host at the subconscious level to prefer foods that contain specific nutrients that favor their growth. Gut microbes that love chocolates or sweets, for example, might motivate the host to eat them more often. “Like microscopic puppetmasters, microbes may control the eating behavior of hosts…,” they reckoned.

To support their scientific viewpoint, Professor Maley and colleagues articulated 5 compelling pieces of evidence.

1. Taste Receptors

Germ-free mice are bred in a sterile environment and, hence, they lack proper gut microbiota. Germ-free mice are one of the best research tools to understand the impact of gut microbiota on the host physiology.

Studies have shown that germ-mice have an increased preference for fatty and sugary foods than normal mice with gut microbiota. And the germ-free mice have a higher expression of receptors for fat and sugar in their mouth and intestines. This suggests that low gut microbial diversity, as reflected in germ-free mice, encourages food preferences for fats and sugars.

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2. The Vagal Tone

In 2008, researchers at Mayo Clinic, Minnesota have successfully applied vagal blockage (vBloc) therapy to treat obesity. Participants consumed 30% fewer calories as a result of quicker satiation and reduced hunger.

The similar weight loss outcomes were replicated in 2016 and in 2017, with the latter study concluding that “vBloc therapy continues to result in medically meaningful weight loss with a favorable safety profile through 2 years.”The Food and Drug Administration (FDA) has, in fact, already approved vBloc therapy for treating obesity in 2015.

The vagus nerve is the main driver of the body’s rest-and-digest activities. It makes sense that an overactive vagus nerve would lead to excessive digestive activities and resulting hunger. Stimulating the vagus nerve with noradrenaline in mice made them desire more food despite already eating beyond the point of satiation; this did not occur if the vagus nerve was cut.

Some gut microbes such as Bacillus and Escherichia species secrete noradrenaline. “Gut microbes that produce adrenergic neurochemicals may [therefore] contribute to overeating via mechanisms involving vagal nerve activity,” Professor Maley and his team wrote.

3. Appetite-Regulating Hormones

Lower levels of satiety hormones (e.g., leptin and cholecystokinin) have been found in germ-free mice. Feeding mice with Lactobacillus probiotics, in turn, inhibited the release of hunger hormones (e.g., agouti-related protein and neuropeptide Y) in the brain.

Certain gut bacteria can synthesize peptides that bear structural similarities to human appetite-regulating peptide hormones such as ghrelin and leptin. The structure of a protein is the chief determinant of which receptor(s) it binds to and consequently what effect(s) it exerts. Thus, these microbial peptides are ‘mimics’ to host’s appetite-regulating peptide hormones, in terms of structure and function.

These microbial peptide mimics, however, are usually silenced by host enzymes — “a phenomenon that could have evolved as a mammalian counter-adaptation to microbial manipulation,” Professor Maley et al. said in a statement. But in case they were not silenced completely, “microbial manipulation” may be in effect.

4. Toxins

Under conditions of nutrients imbalances, microbial communities normally at low levels might bloom. Excessive iron bioavailability in the gut, for instance, increases the populations of pathogenic Salmonella and Candida species that can release toxins and injure the gut.

The resulting gut inflammation could induce a negative mood, leading to emotional eating, the researchers hypothesize. Otherwise, the gut bacterial toxins might also trigger the avoidance of specific foods via the activation of pain receptors present in the gut.

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5. Dietary Preferences

Prevotella grows best on carbohydrates; dietary fiber provides a competitive advantage to Bifidobacteria, and Bacteroidetes has a substrate preference for certain fats,” Professor Maley et al. explained. Whereas Roseburia species thrive with polysaccharides or complex carbohydrates. Japanese natives have evolved a gut bacterium called Bacteroides plebeius that digests seaweed.

These show that gut microbes have food preferences too. It won’t be a surprise if they have evolved mechanisms to improve their fitness (i.e., growth) by influencing the host's dietary choices, for example.

“Modern biology suggests that our bodies are composed of a diversity of organisms competing for nutritional resources,” the researchers wrote. Evolutionary competition between the host vs. gut microbes fitness may lead to “cognitive conflict” in food choices — i.e., food cravings.

“Exerting self-control over eating choices may be partly a matter of suppressing microbial signals that originate in the gut,” Professor Maley and colleagues conclude. “Acquired tastes may [therefore] be due to the acquisition of microbes that benefit from those foods.”

This article was originally published in Microbial Instincts.

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