Microbes Rule Our Guts

Microbes Rule Our Guts

Author: Antonia Niedobitek

Do We Have a Choice of What to Eat And What Not?

Resisting cravings for certain foods, especially when they are the rather unhealthy type, is a common dilemma most of us are confronted with regularly. Health issues like obesity, diabetes and heart disease are tightly linked to unhealthy eating habits. Usually, we associate bad eating habits with a lack of self-discipline and assume that everyone has their own freedom of choice of what to eat and what not. A group of researchers from the USA suggest that our eating behavior might be manipulated by our individual gastrointestinal microbiomes, that is the spectrum of microbial organisms that populate our gut.


Joe Alcock, Carlo Maley and Athena Aktipis hypothesize that evolutionary conflict between the host animal and microbes in the gut leads to contrary interests concerning the nutrition of the host. They review several studies indicating the manipulation of host eating behavior by microbes to promote their fitness at the expense of the host’s fitness. They look at how cravings for certain foods might be connected to the composition of gut microbiota. For example, “chocolate-lovers” were found to have a different spectrum of microbial metabolites in their urine compared with “chocolate indifferent” individuals. There is even evidence that microbes have effects on mood, e.g. probiotic Lactobacillus casei, a lactic acid bacteria species, can improve mood when consumed.


Microbial Diversity

Alcock, Maley and Aktipis speculate that the level of diversity within the microbiome may also be a determining factor for eating behavior. For example, a low level of diversity might be associated with bad eating habits because certain species can reach high population sizes and have more resources available for host manipulation. High diversity, on the other hand, means microbes have to invest more energy in competition. This suggests that a lower diversity of the intestinal microbiome may be associated with an unhealthy eating behavior and possibly greater obesity.


Manipulation of host eating behavior can occur by a range of different mechanisms such as inducing dysphoria and producing hormones, which will be discussed in what follows.


Mechanisms of Manipulation

Microbes can induce dysphoria via expression of bacterial virulence genes, which improve the fitness of the microbe and usually have a pathogenic effect on the host. For example, virulence proteins have been shown to activate pain receptors that act in the human intestinal epithelium and affect the host’s behavior via pain signaling. Another mechanism of manipulation can occur via modulation of host receptor expression. Experiments show that germ-free mice have altered taste receptors and a preference for sweets compared to normal mice.


Microbes may also interfere with the host’s nervous system via the vagus nerve, a central part of the microbiome-brain-axis that connects the nervous system of the gut with the brain. Enteric receptors respond to the presence of certain bacteria and to bacterial metabolites. Blockade or severing of the vagus nerve in humans has been shown to result in drastic weight loss. This means microbes could potentially affect the host’s eating behavior by orchestrating the vagus nerve traffic.


Microbes could potentially also manipulate eating behavior via hormones. They can produce mammalian hormone analogs and elevate concentrations in the host’s blood, or they can reduce levels of certain hormones by other mechanisms. Mice that were fed with a dietary supplement (VSL#3) containing a mix of Lactobacillus strains had lower levels of hunger-inducing hormones AgRP (agouti related protein). Many gut microbes produce peptides that are very similar to leptin, ghrelin or peptide YY, which are regulators of satiety and hunger.


There is evidence that the evolutionary conflict between intestinal microbiome and host is directly linked to the epidemic of obesity. Work with mice that were genetically predisposed to obesity showed that when raised germ-free the animals had normal weight distributions; only upon feeding with fecal pellets from a conventionally raised obese mouse did they become obese themselves. This raises the possibility that food preferences are contagious and that obesity is transmitted by a similar mechanism amongst other animals as well. Additionally, differences in gut microbiota between obese and non-obese humans were found. Microbiomes of obese humans are generally less diverse in comparison to lean individuals.


Modify Your Gut Microbiome

If you are wondering now, what you can do to actively modify your own gut microbiome, probiotics might possibly be the answer. Studies have shown that the uptake of probiotics can cause people to consume less food. This observation supports the hypothesis that higher gut microbe diversity may constrain microbial manipulation of eating behavior. Mice fed with probiotic Bifidobacterium breve showed reduced weight gain although they were given a high fat diet. Similar results were achieved in studies with humans. The question of how exactly we can make use of this convenient feature of probiotics in daily life remains a subject of discussion.



Overall, Alcock, Maley and Aktipis conclude with various predictions. For one thing, a possible strategy to alter an individual’s eating behavior could be the uptake of prebiotics, probiotics, antibiotics etc. Alternatively, inoculation of an animal with a microbe specialized on certain nutrients could result in a preference for a certain food containing those nutrients. Similarly, a consistent diet with a defined range of foods could result in selection for microbes specialized on those foods.


Unfortunately, best practice in approaches for managing the types of microbial commensals that inhabit our guts has yet to be elaborated. The good news is that we probably don’t have to blame ourselves for eating the wrong foods. The kind of food that we crave quite possibly depends on our individual microbiome and isn’t a result of lack of self-control. Developing strategies to alter our personal microbiota could be a key factor for public health issues such as obesity and other related diseases.


  1. Aurelian Udristioiu

    Alcohol dehydrogenase (ADH) is an enzyme that makes it possible for humans to drink beer, wine, and other alcoholic beverages. However, its “real” function is thought to be the conversion of alcohol generated by bacteria in the intestine to other metabolic products. Individuals with some mutant forms of ADH may be especially sensitive to alcohol. The molecule is a dimer made either of two identical or two different chains. Chronic alcohol abuse increases gut permeability resulting in high circulating endotoxin that reaches the liver via portal circulation. Endotoxin (lipopolysaccharide or LPS) is recognized by the Toll-like receptor (TLR)-4 complex on resident macrophages or Kupffer cells in the liver, leading to production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, and resulting in injury to liver cells (hepatocytes).

    While they are not used in routine clinical practice, pro-inflammatory cytokine serum concentrations such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8) have been demonstrated to correlate with mortality in patients with alcoholic hepatitis. Induction of inflammatory cytokines by pathogens is a pivotal step in the host’s immune defence.

    Aurelian Udristioiu¹, Manole Cojocaru²

    ¹Clinical Laboratory, Department of Hematology, Emergency County Hospital Targu Jiu & UCB University, Romania, E-mail: [email protected]

    ²Titu Maiorescu University, Faculty of Medicine, Physiology Department, Bucharest, Romania; E-mail: [email protected]


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