The research essay suggests that evolutionary conflict between our own needs and those of the bacteria that make up our microbiota may lead to cravings and ‘cognitive conflict with regard to food choice.’
Writing in BioEssays, the researchers behind the review noted that it has been suggested that the microbes that call our gastrointestinal tract home are under ‘selective pressure’ to manipulate our own eating behaviour to increase their ability to survive (known as fitness) - sometimes at the expense of our fitness.
“Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness,” they suggested, noting that their review highlights potential mechanisms for microbial control over eating behaviour - including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the neural axis between the gut and the brain.
“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” they suggested.
A walking microbial colony?
Led by Joe Alcock from the University of New Mexico, the team note that microbial genes outnumber human genes by 100 to 1 in the intestinal microbiome, leading some to propose that it is a “microbial organ” that performs important functions for the host, such as nutrient harvesting and immune development.
However, as with any complex and intimate interaction, there is a mixture of common and divergent interests with opportunities for mutual benefit and manipulation, said the team.
"Fitness interests of gut microbes are also often not aligned, because members of the microbiota compete with one another over habitat and nutrients. This means that highly diverse populations of gut microbes may be more likely to expend energy and resources in competition, compared to a less diverse microbial population," suggested Alcock and colleagues.
Indeed, they added that a less diverse microbial population is likely to have species within it that have large population sizes and more resources available for host manipulation.
"Moreover, the larger a particular microbial population is, the more power it would have to manipulate the host through higher levels of factor production or other strategies ... and large scale coordination of these activities," they said.
"Therefore, we hypothesize that lower diversity in gut microbiome should be associated with more unhealthy eating behavior and greater obesity (i.e., decreased host fitness)."
Alcock and his team added that there are a number of existing hypotheses for the prevalence of obesity and our cravings for unhealthy foods, including addiction/lack of willpower, environmental mismatch, and nutrient shortages - adding that a microbial cause is not mutually exclusive of other alternatives such as nutrient deprivation.
Indeed, they suggested that exerting self-control over eating choices may be partly a matter of suppressing microbial signals that originate in the gut.
"Acquired tastes may be due to the acquisition of microbes that benefit from those foods. Our review suggests that one way to change eating behaviour is by intervening in our microbiota," said Alcock and his colleagues. "Until we have a better understanding of the contributions and interactions between individual microbial taxa, it may be more effective to focus interventions on increasing microbial diversity in the gut.”
"Competition between genomes is likely to produce a variety of conflicts, and we propose that one important area, impacting human health, is in host eating behaviour and nutrient acquisition," they concluded.
Published online ahead of print, doi: 10.1002/bies.201400071
“Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms”
Authors: Joe Alcock, Carlo C. Maley, C. Athena Aktipis