Georgia University. US: Emulsifiers, which are added to most processed foods to aid texture
and extend shelf life, can alter the gut microbiota composition and
localization to induce intestinal inflammation that promotes the
development of inflammatory bowel disease and metabolic syndrome, new
research shows.
The research, published Feb. 25 in Nature, was led by Georgia State University Institute for Biomedical Sciences’
researchers Drs. Benoit Chassaing and Andrew T. Gewirtz, and included
contributions from Emory University, Cornell University and Bar-Ilan
University in Israel.
Inflammatory bowel disease (IBD), which includes Crohn’s disease and
ulcerative colitis, afflicts millions of people and is often severe and
debilitating. Metabolic syndrome is a group of very common
obesity-related disorders that can lead to type-2 diabetes,
cardiovascular and/or liver diseases. Incidence of IBD and metabolic
syndrome has been markedly increasing since the mid-20th century.
The term “gut microbiota” refers to the diverse population of 100
trillion bacteria that inhabit the intestinal tract. Gut microbiota are
disturbed in IBD and metabolic syndrome. Chassaing and Gewirtz’s
findings suggest emulsifiers might be partially responsible for this
disturbance and the increased incidence of these diseases.
“A key feature of these modern plagues is alteration of the gut
microbiota in a manner that promotes inflammation,” says Gewirtz.
“The dramatic increase in these diseases has occurred despite
consistent human genetics, suggesting a pivotal role for an
environmental factor,” says Chassaing. “Food interacts intimately with
the microbiota so we considered what modern additions to the food supply
might possibly make gut bacteria more pro-inflammatory.”
Addition of emulsifiers to food seemed to fit the time frame and had
been shown to promote bacterial translocation across epithelial cells.
Chassaing and Gewirtz hypothesized that emulsifiers might affect the gut
microbiota to promote these inflammatory diseases and designed
experiments in mice to test this possibility.
The team fed mice two very commonly used emulsifiers, polysorbate 80
and carboxymethylcellulsose, at doses seeking to model the broad
consumption of the numerous emulsifiers that are incorporated into
almost all processed foods. They observed that emulsifier consumption
changed the species composition of the gut microbiota and did so in a
manner that made it more pro-inflammatory. The altered microbiota had
enhanced capacity to digest and infiltrate the dense mucus layer that
lines the intestine, which is normally, largely devoid of bacteria.
Alterations in bacterial species resulted in bacteria expressing more
flagellin and lipopolysaccharide, which can activate pro-inflammatory
gene expression by the immune system.
Such changes in bacteria triggered chronic colitis in mice
genetically prone to this disorder, due to abnormal immune systems. In
contrast, in mice with normal immune systems, emulsifiers induced
low-grade or mild intestinal inflammation and metabolic syndrome,
characterized by increased levels of food consumption, obesity,
hyperglycemia and insulin resistance.
The effects of emulsifier consumption were eliminated in germ-free
mice, which lack a microbiota. Transplant of microbiota from
emulsifiers-treated mice to germ-free mice was sufficient to transfer
some parameters of low-grade inflammation and metabolic syndrome,
indicating a central role for the microbiota in mediating the adverse
effect of emulsifiers.
The team is now testing additional emulsifiers and designing
experiments to investigate how emulsifiers affect humans. If similar
results are obtained, it would indicate a role for this class of food
additive in driving the epidemic of obesity, its inter-related
consequences and a range of diseases associated with chronic gut
inflammation.
While detailed mechanisms underlying the effect of emulsifiers on
metabolism remain under study, the team points out that avoiding excess
food consumption is of paramount importance.
“We do not disagree with the commonly held assumption that
over-eating is a central cause of obesity and metabolic syndrome,”
Gewirtz says. “Rather, our findings reinforce the concept suggested by
earlier work that low-grade inflammation resulting from an altered
microbiota can be an underlying cause of excess eating.”
The team notes that the results of their study suggest that current
means of testing and approving food additives may not be adequate to
prevent use of chemicals that promote diseases driven by low-grade
inflammation and/or which will cause disease primarily in susceptible
hosts.
This study was funded by the National Institutes of Health and Crohn’s & Colitis Foundation of America.